Rejuvenation Biotechnology 2014 Full Program

August 21-23, 2014
Santa Clara, California
a SENS Research Foundation Conference
Program Guide
a SENS Research Foundation Conference
August 21-23, 2014

Hyatt Regency Hotel
Santa Clara, California
Dear Colleagues,
It is our pleasure to welcome you to the 2014 Rejuvenation Biotechnology Conference.
The continuing growth of research into the underlying causes of the diseases of aging
brings with it the opportunity to build a Rejuvenation Biotechnology industry, an
industry which builds on the strengths of regenerative medicine. Together over the next
three days, we believe we can help create this new industry and inspire each other as
clinicians, researchers, patient advocates, regulators, venture capitalists, investors and
industry leaders to work together to make this happen.
This conference has been designed to offer something for everyone: from the
inspirational words of our scientific, business, and venture capital speakers to the latest
research on diseases, such as Alzheimers Disease, cancer, cardiovascular disease, and
diabetes. An entire track of sessions will cover the regulatory, financial, and economic
issues involved in building a Rejuvenation Biotechnology industry. We have also
scheduled plenty of time for networking with each other during our meal breaks, Poster
sessions and our evening entertainment.
We would like to thank each of your for attending the Rejuvenation Biotechnology
Conference and bringing your expertise to our gathering. You have the vision, the
knowledge, the wherewithal and the experience to come together to pave the way
into the future. Throughout this conference, we ask you to stay engaged, deepen your
understanding of the field, build communities of interest and create collaborations that
will help shape the future of the industry.
Thank you for choosing this conference. Enjoy your time here, and once again welcome to
the Rejuvenation Biotechnology Conference.
Mike Kope
CEO, SENS Research Foundation
Aubrey de Grey
CSO, SENS Research Foundation
Table of Contents
Welcome Letter. . . . . . . . . . . . . . . . . . . . . . . . 2
Conference Schedule . . . . . . . . . . . . . . . . . . . 4
Speaker Biographies. . . . . . . . . . . . . . . . . . . 14
Sponsors . . . . . . . . . . . . . . . . . . . . . . . . . . . 26
Poster Abstracts . . . . . . . . . . . . . . . . . . . . . . 33
H
Networking Meals, Posters and
Exhibits in Ballrooms EFGH
SANTA CLARA
CONVENTION
CENTER
G
F
A
Keynotes, Plenary & Concurrent Panels,
and Performances in Ballrooms ABCD
Ballrooms
B
C
Registration in LOBBY WEST
TUSCA
COURTYARD
ELEVATORS
TUSCA RESTAURANT
TO PARKING STRUCTURE
LOBBY
WEST
RESTROOMS
NAPA I
NAPA II
NAPA III
SONOMA
@ THE MARKET
REGENCY CLUB
FRONT
DESK
RESTROOMS
POOL ELEVATOR
TRUYA SUSHI
LOUNGE
CONCIERGE
GIFT SHOP
CABANAS
MENDOCINO
EVOLUTION
CAFE AND BAR
SWIMMING POOL
TERRA COURTYARD
UP TO BALLROOM
NETWORK
MEETING
CENTER
RESTROOMS
ATM
WHIRLPOOL
MAGNOLIA
HOTEL ENTRANCE
Conference Schedule
Day 1: Thursday, August 21, 2014
8:00 am
Registration (until 5:00 pm) - [LOBBY WEST]
8:00 am
Networking Breakfast - [Ballrooms EFGH]
9:00 am
Opening Remarks - Michael Kope, CEO , SENS Research Foundation - [Ballrooms ABCD]
9:30 am
Keynote: George Church, Professor of Genetics, Harvard Medical School, Professor of Health
Sciences and Technology, Harvard and MIT: New Epigenome Analysis and Engineering
Technologies for Reversal of Aging - [Ballrooms ABCD]
10:30 am
Molecular and Cellular Damage as the Cause of the Diseases of Aging Panel - [Ballrooms ABCD]
This panel will discuss the idea that the diseases of aging may stem from molecular and cellular
damage that accrues with age. Topics of discussion will include the types of damage that may
be involved, examples of how this applies to one or more diseases, and thoughts on how basic
research and industry could use this concept to drive therapeutic target identification and drug
treatment/development.
Richard Barker, Director, Center for the Advancement of Sustainable Medical Innovation:
(Moderator)
Aubrey de Grey, Co-Founder and Chief Science Officer, SENS Research Foundation
Caleb Finch, ARCO/Kieschnick Professor of Gerontology and Biological Science and University
Professor, USC Davis School of Gerontology
Jeff Karp, Associate Professor, Harvard Medical School, Co-Director of the Center for
Regenerative Therapeutics, Brigham and Womens Hospital
Stephen Minger, Chief Scientist, Cellular Sciences, GE Healthcare Life Sciences, UK
12:00 pm
Networking Lunch & Exhibits - [Ballrooms EFGH]
Conference Schedule
1:00 pm
CONCURRENT SESSIONS. PLEASE CHOOSE ONE:

[Ballroom A]
[Ballroom D]
Alzheimers Disease Session 1
Cardiovascular Disease Session 1
This session will highlight two types of

cellular and molecular damage currently
being researched as therapeutic targets for
Alzheimers Disease. Speakers will discuss
how tau tangles and cell loss are believed
to lead to Alzheimers Disease, current
ideas on how to remove or repair tau
tangles, and how cell replacement can be
used to treat Alzheimers.
Building upon the idea discussed by the

morning panel of using damage repair
therapeutics to treat the diseases of aging,
this session will consider cellular and
molecular damage that can be targeted
for cardiovascular disease therapy.
Presentations will explain how cellular or
molecular damage may lead to cardiovascular disease and how this damage may
be removed or repaired.
Jean Hbert, Professor, Departments of

Neuroscience and Genetics, Albert Einstein
College of Medicine: A Twist of Fate Reprogramming Neural Precursor Cells
to Generate New Neocortical Neurons
Einar Sigurdsson, Associate Professor,
Department of Neuroscience &
Physiology, New York University: Tau
Immunotherapy and Imaging
Claude Wischik, Professor of Old Age

Psychiatry, University of Aberdeen,
Executive Chairman, TauRX Therapeutics,
Ltd.: Status of the First Phase 3 Clinical
Trials Targeting the Tauopathy of
Alzheimers Disease: Origins, Rationale
and Design Considerations
Guillermo Garcia Cardena, Associate

Professor of Pathology, Harvard Medical
School, Director of the Laboratory for
Systems Biology, Center for Excellence in
Vascular Biology, Brigham and Womens
Hospital: Mechanical Forces, Vascular
Inflammation and Atherosclerosis
W. Gray Jerome, Associate Professor and
Director, Graduate Program in Cellular
and Molecular Pathology, Vanderbilt
University Medical Center: Chewing
the Fat: Cholesterol, Autophagy and
Lysosome Dysfunction
Michael Sherratt, Lecturer, Center
for Regenerative Medicine,
University of Manchester: Causes
and Consequences of Age-Related
Extracellular Matrix Remodelling
[Ballrooms BC]
Toward a New Investment
Paradigm Panel
This panel will discuss the challenges in
bringing new and especially preventative
therapies to treat the diseases of aging
from the research lab to the market.
The panel will offer and discuss new
investment paradigms that could drive
drug and therapeutic development.
David Brindley, Research Fellow,
University of Oxford/Center for the

Advancement of Sustainable Medical
Innovation: (Moderator)
Neil Littman, Business Development

Officer, California Institute for
Regenerative Medicine
James ONeill, Partner and
Chief Operating Officer, Mithril

Capital Management
Bernard Siegel, Executive Director,

Genetics Policy Institute
Michael West, CEO, BioTime, Inc.
Conference Schedule
Day 1: Thursday, August 21, 2014
2:30 pm

[Ballroom A]
Alzheimers Disease Session 2
Cardiovascular Disease Session 2
A third type of damage being targeted for

Alzheimers therapeutics, A-beta aggregates,
will be discussed during this session. Speakers will address how A-beta aggregates are
believed to lead to Alzheimers Disease and
current ideas on how to prevent or remove
them. This session will also discuss how
changing the way researchers, regulators,
and pharmaceutical companies view the
disease will change Alzheimers Disease
drug development. Particular attention will
be paid to the Accelerate Cure/Treatments
for Alzheimers Disease (ACT-AD) proposal
and recent guidance from the FDA.
In this session, examples of current

pharmaceutical advances in cardiovascular
disease therapeutics will be presented.
The talks will describe how these
therapeutics remove or repair molecular
and cellular damage and, in doing so,
delay or prevent cardiovascular disease.
Ashley Bush, Head of the Oxidation

Disorders Laboratory, Mental Health
Research Institute, University of

Melbourne, Director of the Laboratory
for Oxidation Biology Genetics and
Aging Unit, Massachusetts General
Hospital, Associate Professor,
Department of Psychiatry, Harvard
Medical School: Iron in Aging and
Neurodegenerative Disease
Rachelle Doody, Professor of Neurology,

Director, Alzheimers Disease and Memory
Disorders Center, Baylor College of
Medicine: Approaches to Brain Aging
and Alzheimers Disease: What are We

Learning from Clinical Trials?
Eric Siemers, Medical Director,

Alzheimers Disease Team, Eli Lilly:
New Paradigms in Alzheimers
Disease Drug Development
[Ballroom D]
Gabor Forgacs, Professor, Biophysics
Laboratory, Department of Physics

& Astronomy, University of MissouriColumbia, Founder, Organovo: The Role
of Bioprinting in Rejuvenation
Linda Marban, CEO, Capricor

Therapeutics: Raising Capricor:
Building a Biotech Company
from Bench to Bedside
James Yoo, Professor, Associate Director
and Chief Scientific Officer, Wake Forest
Institute for Regenerative Medicine:
Tissue Engineering Solutions for

Cardiovascular Tissue Pathologies
[Ballrooms BC]
The Economic Impact of an Aging
Population on the Healthcare
System Panel
This panel will discuss the impending
economic crisis the healthcare system
will soon face caring for the ever-growing
elderly population and possible solutions
to this crisis, such as an outcomes-based
healthcare model.

Catalina Hoffman, Founder, Catalina

Hoffmann Holding Group
Peter Nakada, Managing Director of Risk

Markets, Risk Management Solutions, Inc.
Conference Schedule
4:00 pm
Afternoon Break & Exhibits - [Ballrooms EFGH]
4:30 pm
Advancing Regenerative Therapies in Alzheimers and Cardiovascular Disease Panel - [Ballrooms ABCD]
This panel will bring together speakers from sessions throughout the day to consider the promise
of a damage repair strategy to develop therapeutics for the diseases of aging. Discussion will
include a summary of the accomplishments of the Alzheimers community in suggesting an
innovative drug development strategy as well as debate about how such a strategy could
apply to cardiovascular therapies. In particular, the panel will consider the impact applying
a strategy similar to the ACT-AD proposal would have on cardiovascular disease therapeutic
development, investment in cardiovascular drug development, and the healthcare system.
Aubrey de Grey, CSO, SENS Research Foundation: (Moderator)

Rachelle Doody, Professor of Neurology, Director, Alzheimers Disease and Memory Disorders
Center, Baylor College of Medicine
Neil Littman, Business Development Officer, California Institute for Regenerative Medicine (CIRM)
Linda Marban, CEO, Capricor Therapeutics
Eric Siemers, Medical Director, Alzheimers Disease Team, Eli Lilly
6:00 pm
Poster Session/ Buffet Dinner & Exhibits - [Ballrooms EFGH]
8:00 pm
Performance by Comedian Hal Sparks - [Ballrooms ABCD]

Currently starring in the Disney XD show, LAB RATS, actor/comedian Hal Sparks began his
professional career while still a teenager in Chicago. As a member of the famed Second City
Troupe, his quick wit and affable personality quickly gained him recognition and acclaim
and he was named the Funniest Teenager In Chicago by the Chicago Sun Times. Sparks
went on to host the Emmy Award- winning Talk Soup on E! Entertainment Television,
winning rave reviews from fans and critics alike. He starred for five seasons on Showtimes
hit series Queer As Folk and appeared in the films Extract, Spiderman 2 and Dude,
Wheres My Car?. Sparks recently starred in his own one hour Showtime comedy special,
Charmageddon, which is now a best-selling DVD. He is a star commentator on VH1s popular
I Love the 80s series and can be heard every Wednesday on the nationally syndicated
Stephanie Miller Radio Show. Hal is also a pop culture expert and regularly appears on such
shows as Joy Behar and CNNs Your Money. His numerous other television appearances
include The Tonight Show, Larry King Live, Charlie Rose, Good Morning America, The
View, Jimmy Kimmel and MTV. In addition to a busy acting and stand-up career, he is an
accomplished musician. Hal and his band, Zero 1, recently released their debut album.
Conference Schedule
Day 2: Friday, August 22, 2014
8:00 am
Registration (until 5:00 pm) - [LOBBY WEST]
8:00 am
Networking Breakfast & Exhibits - [Ballrooms EFGH]
9:00 am
Opening Remarks by Edward James Olmos, Actor - [Ballrooms ABCD]
9:30 am
Keynote: Jim ONeill, Partner and Chief Operating Officer, Mithril Capital Management:
Fight Aging with a Durable Business - [Ballrooms ABCD]
10:30 am
Toward a New Research Paradigm Panel - [Ballrooms ABCD]

This panel will explore new ways to approach research to tackle the diseases of aging. In particular,
consideration will be given to the effects a damage repair paradigm would have on developing
new strategies to identify and study therapeutic targets, fostering more collaboration between
researchers studying different diseases, and changing the way translational research and drug
development are approached.
(Moderator)
Julie Allickson, Director, Translational Research, Wake Forest Institute for Regenerative Medicine
Judith Campisi, Professor, Buck Institute for Research on Aging
Howard Foyt, Vice President, Clinical Development and Chief Medical Officer, Viacyte, Inc
Daniel Kraft, Faculty Chair for Medicine, Singularity University
12:00 pm
Conference Schedule
1:00 pm

[Ballroom A]
[Ballroom D]
Cancer Session
Parkinsons Disease Session
This session will highlight current breakthroughs in cancer research. Additionally,

the impact the I-SPY TRIAL 2 (Investigation
of Serial studies to Predict Your Therapeutic
Response with Imaging and Molecular
Analysis 2) program has had on drug
development, particularly Alzheimers
drugs, will be discussed.
This session will feature the latest in

Parkinsons Disease research. A causal
relationship between molecular and/
or cellular damage and Parkinsons
Disease will be explored. The speakers
will also consider how this research
could lead to preventative or damage
repair treatment of the disease.
Judith Campisi, Professor, Buck Institute

for Research on Aging: Cancer and
Aging: Rival Demons?
Julie Andersen, Professor, Buck Institute

for Research on Aging: Senescence and
the Aging Brain
Laura Esserman, Professor, Departments
Jeanne Loring, Professor, Scripps

Research Institute: Negotiating the
Mine Field in the Quest for a Parkinsons
Disease Cell Therapy
of Surgery and Radiology, and Affiliate

Faculty, Institute for Health Policy
Studies and Director, Carol Franc Buck
Breast Care Center; Co-Leader, Breast
Oncology Program, UCSF Helen Diller
Family Comprehensive Cancer Center,
University of California, San Francisco:
Accelerating Knowledge Turns: The

I-SPY Model and Drug Development
Dale Schenk, CEO, Prothena

Corporation: Challenges and Hopes in
Preventing and Developing Meaningful
Therapeutic Strategies for Alzheimers
and Parkinsons Diseases
Claudia Gravekamp, Associate Professor,

Albert Einstein College of Medicine:
Curing Cancer in the Elderly Through
Novel Strategies
[Ballrooms BC]
Risk-Benefit Analysis in Therapies for
the Diseases and Disabilities of Aging
Today, the translation of healthcare
innovations into patient outcomes is
an inherently multi-stakeholder effort.
Consequently, there is a major need to
maintain rigor and independence in the
regulation of healthcare innovations,
while improving regulatory transparency
and opportunities for multi-stakeholder
input to accommodate fundamental
changes in the life-science ecosystem and
global healthcare demands. A key strategy
in this endeavor is the development and
utilization of novel risk-benefit appraisal
methodologies, leveraging advances
in patient reported outcomes (PROMS),
stratified medicines including big data
and risk management methodologies
utilized presently in other industries.

Richard Barker, Director, Center for

the Advancement of Sustainable
Medical Innovation
Chris Hornsby, Head of Model

Development, Life Risks, Risk
Management Solutions, Inc.
Brock Reeve, Executive Director, Harvard

Stem Cell Institute
2:30 pm
Afternoon Break & Exhibits - [Ballrooms EFGH]
Conference Schedule
Day 2: Friday, August 22, 2014
3:30 pm
Advancing Regenerative Therapies in Cancer and Parkinsons Disease Panel - [Ballrooms ABCD]
This panel will bring together speakers from throughout the day to summarize the impact of
the I-SPY TRIAL 2 program on drug trial design for Alzheimers therapeutics and speculate on
the applicability of trial designs similar to the one proposed for Alzheimers Disease to the
development of therapeutics for other diseases of aging, such as Parkinsons Disease and cancer.

Rachelle Doody, Professor of Neurology, Director, Alzheimers Disease and Memory Disorders
Center, Baylor College of Medicine
Laura Esserman, Professor, Departments of Surgery and Radiology, and Affiliate Faculty,
Institute for Health Policy Studies and Director, Carol Franc Buck Breast Care Center; Co-Leader,
Breast Oncology Program, UCSF Helen Diller Family Comprehensive Cancer Center, University
of California, San Francisco
Jeanne Loring, Professor, Scripps Research Institute

Brock Reeve, Executive Director, Harvard Stem Cell Institute
Dale Schenk, CEO, Prothena Corporation
5:30 pm
Networking Dinner/ Poster Session & Exhibits - [Ballrooms EFGH]
8:00 pm
Performance by Comedian Dan Nainan - [Ballrooms ABCD]

Dan Nainan got his start by taking a comedy class to get over the nervousness of speaking
on stage in his job as a demo engineer with Intel Corporation. After leaving Intel to pursue
comedy, he has toured with Russell Peters and other notable comedians. Dan has appeared
on network television including Last Comic Standing as well as in feature films, on radio
and in an Apple commercial. He just completed a comedy tour of India.
Concert by Cecilia Nol

Originally from Lima, Per, Cecilias career began at the age of eight with a starring role in a
Peruvian television show. As a teenager, Cecilias mother sent her to Argentina and Germany
to take voice, violin, and piano lessons. Encouraged by the legendary Stan Getz to move to the
US, Cecilia relocated to New York City and briefly performed as a dancer with Jo Jos Dance
Factory and Menudo. Cecilia moved to Los Angeles in 1989 and in the early 1990s formed
Cecilia Nol and The Wild Clams. The group received quick attention for their explosive live
shows and were consequently booked at the House of Blues and the Playboy Jazz Festival.
Critics have long called her the Latin Tina Turner. Salsoul, the genre Cecilia created to
describe her sound, combines elements of salsa, soul, jazz, funk, and Afro-cuban. Cecilia also
performs and records with husband and former Men At Work frontman Colin Hay.
10
Conference Schedule
Day 3: Saturday, August 23, 2014
8:00 am
Networking Breakfast & Exhibits - [Ballrooms EFGH]
9:00 am
Keynote: Peter Diamandis, Co-founder and Vice Chairman, Human Longevity, Inc, Founder and
CEO, X PRIZE Foundation: Creating a Culture of Innovation and Breakthroughs - [Ballrooms ABCD]
10:00 am
Applying a Damage Repair Paradigm to Developing Therapies for the Diseases of Aging
Panel - [Ballrooms ABCD]
Building upon the discussion of a damage repair paradigm from days 1 and 2, this panel will weigh
the benefits of application of a damage repair paradigm to drug development to combat the
diseases of aging. Discussion will include the feasibility of applying such a strategy, the advantages
and disadvantages such a model would confer, and an analysis of the regulatory changes that
would be required to make such a paradigm possible.
(Moderator)
Julie Allickson, Director, Translational Research, Wake Forest Institute for Regenerative Medicine
Evan Snyder, Director, Center for Stem Cell and Regenerative Medicine, Director, Stem Cell Research
Center and Core Facility, Sanford-Burnham Medical Research Institute
11:30 am
11
Conference Schedule
Day 3: Saturday, August 23, 2014
12:30 pm

[Ballroom A]
[Ballroom D]
Musculoskeletal Disease Session
Diabetes Session
This session will highlight current musculoskeletal disease research. Presenters will
discuss how molecular or cellular damage
is believed to lead to their musculoskeletal
disease of interest and how their research
may contribute to delaying or preventing
the disease.
Breakthroughs in diabetes research will be

presented in this session. The molecular
and cellular causes of diabetes will be
considered and strategies to remove, repair,
or replace such damage will be discussed.
Christy Carter, Assistant Professor,
Department of Aging and Geriatric

Research, Institute on Aging, University of
Florida: What is Sarcopenia? Definitions,
Diagnosis and Developing Interventions
Young Jang, Assistant Professor,
Georgia Institute of Technology: The
Rejuvenation of Aged Skeletal Muscle

by Systematic Factors
Camillo Ricordi, Stacy Joy Goodman
Professor of Surgery, Distinguished Professor

of Medicine, Director, Diabetes Research
Institute and Cell Transplant Program,
University of Miami: Cellular Therapies
and Regenerative Medicine Strategies

for Treatment of Diabetes
David Schaffer, Professor, University of

California, Berkeley, Director, Berkeley
Stem Cell Center: Molecular Elucidation
and Engineering of Stem Cell Therapies
for the Nervous System
[Ballrooms BC]
Regulating a Damage Repair
Approach to Cure the Diseases of
Aging Panel
Escalating societal healthcare needs have
driven an unprecedented era of biomedical
innovation. However, the development of
candidate technologies without consideration of a robust regulatory strategy is likely
to contribute to stymied patient access and
commercial viability. Therefore, this session
will consider worldwide efforts to rapidly
and proportionally develop international
regulatory processes to accommodate
increasingly heterogeneous and unfamiliar
healthcare technologies and their swift
translation from lab to bedside.

Bob Clay, Chief Regulatory Officer,

Kinapse & Manging Director, Highbury
Regulatory Science
Andrew Martello, Managing Director,

Spoonful of Sugar
Evan Snyder, Director, Center for
Stem Cell and Regenerative Medicine,

Director, Stem Cell Research Center
and Core Facility, Sanford-Burnham
Medical Research Institute
12
Conference Schedule
1:30 pm
Break
2:00 pm
Advancing Regenerative Therapies in Musculoskeletal Disease and Diabetes Panel - [Ballrooms ABCD]
This panel will bring together speakers from the morning sessions to consider the possibility of
applying a drug trial design similar to the ones emerging from the Alzheimers Disease and cancer
communities. The feasibility of applying such a model will be considered with the biology of the
disease, regulatory concerns, and pharmaceutical needs in mind.

Christy Carter, Assistant Professor, Department of Aging and Geriatric Research, Institute on
Aging, University of Florida
Andrew Martello, Managing Director, Spoonful of Sugar

Camillo Ricordi, Stacy Joy Goodman Professor of Surgery, Distinguished Professor of Medicine,
Director, Diabetes Research Institute and Cell Transplant Program, University of Miami
Young Jang, Assistant Professor, Georgia Institute of Technology
3:00 pm
Building a Rejuvenation Biotechnology Industry - [Ballrooms ABCD]

This panel will synthesize the discussions from all of the conference sessions and panels. A crosssection of academics, pharmaceutical reps, policy makers, and other presenters will revisit the
merits of a damage repair paradigm to address the diseases of aging considered at this conference.
Panelists will consider the changes that would be required to lay the groundwork for a new industry
perspective focused on addressing damage indications for the diseases of aging either through
preventing or repairing such damage.
Michael Kope, CEO, SENS Research Foundation: (Moderator)

George Church, Professor of Genetics, Harvard Medical School, Professor of Health Sciences
and Technology, Harvard and MIT
Dana Goldman, Leonard D. Schaeffer Chair and Director of the Schaeffer Center for Health Policy
and Economics, University of Southern California

Brock Reeve, Executive Director, Harvard Stem Cell Institute
4:30 pm
Conference Concludes
13
Speaker Biographies
Julie Allickson
Dr. Allickson focuses

on the translation of
regenerative
medicine products
including cell
therapy, tissue
engineering,
biomaterials and
devices. This process
begins at Proof-ofConcept where early discussions with
regulators and clinicians are critical in
moving the technology from the bench to
the bedside.
Prior to joining the institute, she was an

Executive Officer of the company and Vice
President of Laboratory Operations and
R & D at Cryo-Cell International, Inc., an
AABB accredited Cord Blood Bank. Prior to
this position, she worked for the University Of Miami School Of Medicine, Diabetes Research Institute as the Laboratory
Director of the cGMP Hematopoietic Cell
Processing Facility. She was responsible
for the design and implementation of the
State Licensed Clinical Flow Cytometry
Laboratory.
Dr . Allickson was the lead in Regulatory
Affairs for the processing laboratory of Islet
and Hematopoietic Cell products which
included oversight of all Investigational
New Drugs (IND) and external regulations.
Prior to this, she worked for the American
Red Cross managing the Hematopoietic
Cell Processing and Platelet Serology
Laboratory and serving as a member of the
National Stem Cell Task Force.
She has a Doctorate in Health Sciences and
a Masters Degree in Medical Laboratory
Sciences. She is one of the founding members of the International Society of Cellular
Therapy and a member of the American
Association of Blood Banks (AABB) for 25
years. She is currently Chair of the AABB
Standards Committee for Cell Therapy
Product Services. Dr. Allickson is also on
the Technical Advisory Board for Tissue
Engineered Products under ICCBBA and the
ISCT Commercialization Committee.
14
Julie Andersen
As a renowned
expert on Parkinsons disease, Dr.
Andersen is
pursuing a wide
array of leads
toward treatments
for this complex
neurodegenerative
disorder. She has
identified several early risk signals for
Parkinsons, an age-related illness that
causes a progressive decline in movement
and muscle control. The symptoms can
include shaking hands and difficulty with
walking.
Amongst the early risk signals identified

by Dr. Andersen are elevated levels of iron
and declining amounts of a protective
antioxidant called glutathione. Recently,
the Andersen lab has also discovered
valuable clues by examining the roles
of enzymes and other proteins involved
in nerve cell degeneration. Normally,
proteins carry out the routine work inside
cells. But some enzymes can promote the
symptoms of Parkinsons disease. Blocking
those enzymes might slow down the
disease. Other therapies might result from
the opposite tactic: reinforcing the work
of different enzymes that guard against
Parkinsons disease. These enzymes seem
to prevent damage to genes that protect
the nervous system.
The Andersen lab is also involved in identifying potential biomarkers for Parkinsons
that may allow early interventional therapy.
Dr. Andersen earned a doctorate in
Neuromolecular Biology at the University
of California, Los Angeles (UCLA). She
completed a postdoctoral fellowship at
Harvard Medical School and Massachusetts
General Hospital before going to the
University of Southern California as an
assistant then an associate professor at the
Andrus Gerontology Center. She joined the
Buck Institute in 2000.
Richard Barker
Richard is a strategic
advisor, speaker and
author on healthcare and life
sciences. He is
Director of the
Centre for the
Advancement of
Sustainable Medical
Innovation, a major
European initiative aimed at transforming
the R&D and regulatory processes in life
sciences to bring advances more rapidly
and affordably to patients.
He is also chairman of the South London
Academic Health Science Network, accelerating innovation in this region of the
NHS, and Chairman of Stem Cells for Safer
Medicines, a public-private partnership
developing stem cell technology for
predicting the safety profile of new medicines. He is a board member of Celgene, a
major US-based bio-therapeutics company
and of iCo Therapeutics, a Canadian
bioscience company.
His 25-year business career in healthcare
has spanned biopharmaceuticals, diagnostics and medical informatics both in
the USA and Europe. Most recently he was
Director General of the Association of the
British Pharmaceutical Industry, member
of the Executive Committee of EFPIA (the
European industry association) and Council
member of IFPMA (the international
equivalent).
As a co-founder of Life Sciences UK,
member of the NHS Stakeholder Forum,
vice-chair of the UK Clinical Trials Collaboration and in many other roles, he has
advised successive UK governments on
healthcare issues, especially those relating
to developing, valuing and using new
healthcare technologies.
His past leadership roles include head of
McKinseys European healthcare practice,
General Manager of Healthcare Solutions
for IBM and Chief Executive of Chiron
Diagnostics. He was also Chairman and
Chief Executive of Molecular Staging, a US
bioscience company, now part of Qiagen.
Speaker Biographies
David Brindley
David is an international thoughtleader in the

translation of
life-science
innovations into
commercially viable
products and
services. His
expertise spans the
Valley of Death, encompassing regulation,
engineering and finance. Currently Davids
professional activities include: research into
the optimization of risk: benefit appraisal
techniques for healthcare innovations,
leading the CASMI Translational Stem Cell
Consortium and providing timely and
pragmatic advice to a range of stakeholders
in healthcare translation, notably the
venture capital community.
Examples of Davids work can be found in
a range of high impact journals including
Nature, Nature Biotechnology, Nature Medicine and Cell Stem Cell. David also produces
a popular blog, Cell Therapy Industry 2027,
with the Centre for the Commercialisation
of Regenerative Medicine. David is an
active Fellow of the Royal Institution of
Great Britain and the Royal Society for the
Advancement of Arts and Manufacturing.
David has successfully passed the Charted
Analyst in Alternative Investments (CAIA)
Level 1 examination.
David completed his undergraduate studies
in Biochemical Engineering at University
College London (with First Class Honors) and
his Masters, investigating the commercialization of regenerative therapies, jointly at
the Harvard Stem Cell Institute and Harvard
Business School. Currently he is pursuing a
DPhil (PhD) in Musculoskeletal Sciences at
the University of Oxford.
Ashley Bush
Ashley I. Bush (MB

BS, DPM, FRANZCP,
PhD, FTSE) heads
the Oxidation
Biology Unit at the
Florey Institute of
Neuroscience &
Mental Health, is
Professor of
Neuroscience and
Pathology at The University of Melbourne,
NHMRC Australia Fellow, co-director of
biomarker development for the Australian

Imaging Biomarker Lifestyle Study (AIBL),
Chief Scientific Officer of the Cooperative
Research Center for Mental Health, and has
staff appointments in Psychiatry and Radiology at the Massachusetts General Hospital.
He has received numerous awards including the Potamkin Prize and the Beeson
Award. Professor Bush has authored over
300 publications, with >21,000 citations
(the most highly-cited Australian neuroscientist of the last 10 years), 23 patents and
founded 4 biotechnology companies. His
lab discovered the interaction of beta-amyloid with transitional metals as a major
factor in Alzheimers disease pathology, as
well as the roles of APP and tau in neuronal
iron homeostasis.
Judith Campisi
Judith Campisi
received a PhD in
Biochemistry from
the State University
of New York at Stony
Brook, and postdoctoral training in
cell cycle regulation
and cancer at the
Dana-Farber Cancer
Institute and Harvard Medical School. As an
Assistant Professor at the Boston University
Medical School, she began to focus her
laboratory on role of cellular senescence in
suppressing the development cancer, but
soon became convinced that senescent cells
also contributed to aging. She left Boston
University as an Associate Professor to
accept a Senior Scientist position at the
Lawrence Berkeley National Laboratory in
1991. In 2002, she established a laboratory
at the Buck Institute for Age Research,
where she is a Professor.
At both institutions, Campisi established
a broad program to understand various
aspects of aging, with an emphasis on the
interface between cancer and aging. Her laboratory made several pioneering discoveries
in these areas. Her research continues to
challenge and alter existing
In recognition of the quality of her research
and leadership, Campisi received numerous
awards, including two MERIT awards from
the US National Institute on Aging, awards
from the AlliedSignal Corporation, Gerontological Society of America and American
Federation for Aging Research, and the

Longevity prize from the IPSEN Foundation.
She serves on numerous national and
international editorial and advisory boards.
Guillermo Garca-Cardea
Guillermo Garcia
Cardena is an
Associate Professor
of Pathology at
Harvard Medical
School, and the
Director of the
Laboratory for
Systems Biology at
the Center for
Excellence in Vascular Biology, Brigham and
Womens Hospital, Boston. He received his
Ph.D. degree from Yale University, working
with William C. Sessa on the molecular
regulation of nitric oxide production in
vascular endothelium. His postdoctoral
research with Michael A. Gimbrone Jr. at
Harvard Medical School was on studies of
endothelial cell gene expression, hemodynamics, and atherogenesis.
Christy Carter
Dr. Carter received

her PhD in Experimental and Biological Psychology from
the University of
North Carolina at
Chapel Hill and her
post-doctoral
training at The Wake
Forest University
School of Medicine in Winston-Salem,
North Carolina.
Globally , Dr. Carters current research interests lie in preserving physical function and
healthspan during aging; and in particular
focuses on the use of a preclinical rodent
model of aging to test a variety of late-life
interventions designed to mitigate sarcopenia. Furthermore, she has demonstrated
that the application of standardized physical
performance measures to a variety of animal
models of aging may help to define similarities between species in the underlying
mechanisms of sarcopenia, the age-related
decline in performance, disability, and
longevity. Indeed the assessment of behavioral outcomes is essential for measuring the
efficacy of any late-life intervention in the
context of mitigating declining performance
and improving healthspan. She has extended
15
Speaker Biographies
this area of research to other special aging
populations such as the frail and obese, and
has developed combinatorial therapies,
using these compounds in conjunction with
behavioral modification such as exercise.
George Church
George Church is
Professor of Genetics
at Harvard Medical
School and Director
of PersonalGenomes.
org, which provides
the worlds only
open-access
information on
human Genomic,
Environmental & Trait data (GET). His 1984
Harvard PhD included the first methods for
direct genome sequencing, molecular
multiplexing & barcoding. These led to the
first genome sequence (pathogen, Helicobacter pylori) in 1994. His innovations have
contributed to nearly all next generation
genome sequencing methods and companies (CGI, Life, Illumina, nanopore). This plus
chip-based DNA synthesis and stem cell
engineering resulted in founding additional
application-based companies spanning
fields of medical diagnostics (Knome,
Alacris, AbVitro, Pathogenica ) and synthetic
biology / therapeutics ( Joule, Gen9, Editas,
Egenesis, enEvolv, WarpDrive).
He has also pioneered new privacy, biosafety , environmental & biosecurity policies.
He is director of NIH Center for Excellence
in Genomic Science. His honors include
election to NAS & NAE & Franklin Bower
Laureate for Achievement in Science. He has
coauthored 330 papers, 60 patents & one
book (Regenesis).
Bob Clay
Bob Clay recently

established his own
regulatory consultancy practice
through Highbury
Regulatory Science,
prior to this he was
a VP Global
Regulatory Affairs
at AstraZeneca with
responsibility for oncology, infection and
personalised healthcare. Bob is Chief
Regulatory Officer at Kinapse and a
member of the board of TOPRA. He is a
member of the Expert Scientific Advisory
16
Committee for Medicines for Malaria Venture

(MMV) and several working groups at CPTR
(Critical Path for TB Regimens). He has an
interest in the impact of regulation on the
development of innovative medicines and
healthcare policy matters.
Bob is a regulatory strategist with more than
30 years experience in drug development,
leading the global regulatory approval of
products across a range of therapy areas
including metabolic diseases, neuroscience,
cancer and infection. Bob graduated in
Pharmacy from the University of Bath and
subsequently completed an MSc in BioPharmacy, from the University of London, and an
MBA, from the Open University. Following
completion of his professional training in
hospital pharmacy he joined the pharmaceutical industry as a formulation scientist
at the UK laboratories of Rhone-Poulenc.
Later, he joined the UK Licensing Authority
as a pharmaceutical assessor and has held
regulatory affairs leadership roles with
several pharmaceutical companies including
Wellcome, Zambon, Pfizer and AstraZeneca.
Aubrey de Grey
Dr. de Grey is the

biomedical gerontologist who
researched the idea
for and founded
SENS Research
Foundation. He
received his BA in
Computer Science
and Ph.D. in Biology
from the University of Cambridge in 1985
and 2000, respectively. Dr. de Grey is
Editor-in-Chief of Rejuvenation Research, is a
Fellow of both the Gerontological Society of
America and the American Aging Association,
and sits on the editorial and scientific
advisory boards of numerous journals and
organizations. He is the Chief Science Officer
of the SENS Research Foundation.
Peter Diamandis
Dr. Peter H. Diamandis

is an international
pioneer in the fields of
innovation, incentive
competitions and
commercial space.
In the field of
Innovation, Diamandis
is Chairman and CEO
of the X PRIZE Foundation, best known for its

$10 million Ansari X PRIZE for private
spaceflight. Today the X PRIZE leads the world
in designing and operating large-scale global
competitions to solve market failures.
Diamandis is also the Co-Founder and
Vice-Chairman of Human Longevity Inc. (HLI),
a genomics and cell therapy-based diagnostic and therapeutic company focused on
extending the healthy human lifespan. He is
also the Co-Founder and Executive Chairman
of Singularity University, a graduate-level
Silicon Valley institution that studies exponentially growing technologies, their ability
to transform industries and solve humanitys
grand challenges.
In the field of commercial space, Diamandis
is Co-Founder/Co-Chairman of Planetary
Resources, a company designing spacecraft
to enable the detection and mining of
asteroid for precious materials.
Diamandis is the New York Times Bestselling
author of Abundance The Future Is Better
Than You Think. Abundance was #1 on
Amazon and #2 on New York Times. He was
also named one of The Worlds 50 Greatest
Leaders by Fortune Magazine.
He earned an undergraduate degree in
Molecular Genetics and a graduate degree in
Aerospace Engineering from the Massachusetts Institute of Technology, and received his
M.D. from Harvard Medical School.
Diamandis mission is to open the space
frontier for humanity. His personal motto is:
The best way to predict the future is to create
it yourself.
Rachelle Doody
Dr. Doody is the Effie

Marie Cain Chair in
Alzheimers Disease
Research and
Professor of
Neurology at Baylor
College of Medicine,
where she directs
the Alzheimers
Disease and Memory
Disorders Center (ADMDC). She received a B.A.
from Rice University, a M.D. from Baylor
College of Medicine, and completed internship and residency training at the Royal
Victoria Hospital and Montreal Neurologic
Institute in Montreal, and at Baylor College of
Speaker Biographies
Medicine and has a Ph.D. in Cognitive
Anthropology from Rice University where she
studied the brain and language.
She has published over 170 original research
articles, most dealing with the diagnosis,
progression, or treatment of Alzheimers
Disease. She has received multiple research
grants, including a Zenith Award from
the National Alzheimers Association, and
designed and conducted numerous clinical
trials of Alzheimers Disease therapies. She
participates in National and International
collaborative efforts, review boards, and
advisory boards including Steering
Committees for the NIH AD Cooperative
Study and AD Neuroimaging Initiatives, and
the Steering Committee for the Texas AD
Research and Care Consortium.
Current research interests include studies to
understand and model the progression of
Alzheimers Disease, studies of clinical heterogeneity, and research and development
of new medications to treat Alzheimers
Disease. She works with many biopharmaceutical and large pharma collaborators in
the assessment and experimental testing of
a diverse group of potential AD therapies.
She has served on the Texas Council on
Alzheimers Disease and Related Disorders,
and the Board of Directors for the Houston
and Southeast Texas Chapter of the Alzheimers Association.
Laura Esserman
Dr. Esserman is a
surgeon and breast
cancer oncology
specialist, and is the
Director of the Carol
Franc Buck Breast
Care Center at the
University of
California, San
Francisco (UCSF). In
1996, she started the Center of Excellence for
Breast Cancer Care at UCSF to integrate
clinical care and research, automate tools for
the capture of patient and clinical data, and
develop systems to tailor care to biology,
patient preference, and performance.
Dr. Esserman is nationally and internationally
known as a leader in the field of breast
cancer and has published over 200 articles.
She served as a member of a taskforce for
President Obamas Council of Advisors on
Science and Technology (PCAST) Working
Group on Advancing Innovation in Drug

Development and Evaluation. The group was
tasked with making recommendations to
the federal government about how to best
support science-based innovation in the
process of drug development and regulatory
evaluation.
She is the Principle Investigator of the I-SPY
TRIAL program, a multi-site neoadjuvant
clinical trial (which includes phase 2 and
3 trials) that has evolved into a model for
translational research and innovation in
clinical trial design. Dr. Esserman has recently
launched a University of California-wide
breast cancer initiative called the Athena
Breast Health Network, a program designed
to follow 150,000 women from screening
through treatment and outcomes, incorporating the latest in molecular testing and
web-based tools into the course of care.
Athena is in the final stages of launching a
statewide demonstration project and phase
1/2 trial of personalized screening.
Caleb Finch
Caleb Finch Ph.D. is

ARCO Professor of
Gerontology and
Biological Sciences
at the University of
Southern California,
with adjunct
appointments in the
Department of
Anthropology,
Molecular Biology, Neurobiology, Psychology, Physiology, and Neurology. Major
research interest is the neurobiology of
aging and human evolution. Finch received
his undergraduate degree from Yale in 1961
(Biophysics) and Ph.D. from Rockefeller
University in 1969 (Biology).
His life work is the fundamental biology of
human aging, started in grad school and
continued since 1972 at USC. Discoveries
include a new form of neurotoxicity of
amyloid peptides relevant to Alzheimer
disease and the role of shared inflammatory
pathways in normal and pathological aging
process. Fifteen of his mentored students
hold senior positions in universities or
pharmaceutical corporations.
Finch has received most of the major awards
in biomedical gerontology, including the
Robert W. Kleemeier Award (1985), the
Sandoz Premier Prize (1995), and the Irving
Wright Award (1999). He was founding

Director of the NIA-funded USC Alzheimer
Disease Research Center (1984), and
continues as coDirector and coPI. He also
co-founded Acumen Pharmaceuticals,
which develops therapeutics for Alzheimer
disease. He has written four books, most
recently, The Biology of Human Longevity:
Inflammation and Nutrition in the Evolution
of Lifespans (Academic Press, 2007). Recent
interests include the paleopathology of
human aging and emerging environmental
factors in aging, particularly air pollution
components from fossil fuels.
Gabor Forgacs
Dr. Gabor Forgacs is

a theoretical
physicist turned
bioengineer turned
innovator and
entrepreneur. He is
the George H.
Vineyard Professor of
Biological Physics at
the University of
Missouri-Columbia, the Executive and
Scientific Director of the Shipley Center for
Innovation at Clarkson University and
scientific founder of Organovo, Inc. and
Modern Meadow, Inc.
He was trained as a theoretical physicist

at the Roland Eotvos University, Budapest,
Hungary and the Landau Institute of
Theoretical Physics, Moscow, USSR. He
also has a degree in biology. His research
interests span from topics in theoretical
physics to physical mechanisms in early
embryonic development.
He is the co-author of the celebrated
text in the field, Biological Physics of
the Developing Embryo (Cambridge
University Press, 2005) that discusses the
fundamental morphogenetic mechanisms
evident in early development. These
mechanisms are being applied to building
living structures of prescribed shape and
functionality using bioprinting, a novel tissue engineering technology he pioneered.
He is the author of over 160 peer-reviewed
scientific articles and 5 books.
He has been recognized by numerous
awards and citations. In particular, he
was named as one of the 100 most
innovative people in business in 2010 by
FastCompany.
17
Speaker Biographies
Howard Foyt
Howard Foyt, M.D.,

Ph.D. FACP, Vice
President, Clinical
Development and
Chief Medical Officer
at ViaCyte, Inc., has
over 18 years of
clinical development
experience in
pharmaceutical and
biotechnology environments. Dr. Foyts
background as an endocrinologist and his
multiple NDA and IND applications
position him as ViaCytes strategic leader
for clinical and regulatory operations. Prior
to ViaCyte, Dr. Foyt served as Senior Vice
President and Chief Medical Officer at
Cebix, Inc., a company focused on treatments for complications of type 1 diabetes.
Before Cebix, he was Vice President,
Clinical Development at Metabasis
Therapeutics, Inc. Dr. Foyts pharmaceutical
experience includes senior positions at
Pfizer Global Research & Development and
Parke-Davis Pharmaceutical Research.
As a clinician, Dr. Foyt was Assistant
Professor and Medical Director of
the University Diabetes Center at the
University of Texas Medical Branch. He
earned his medical degree from Baylor
College of Medicine where he also earned
a Ph.D. in Cell Biology. Dr. Foyt completed
his residency in internal medicine at
Baylor and an endocrinology fellowship
at the National Institute of Diabetes and
Digestive and Kidney Diseases, National
Institutes of Health.
Dana Goldman
Dana Goldman is a
Professor and the
Leonard D. Schaeffer
Chair in Health
Policy at the
University of
Southern California.
He is also the
inaugural director of
the Schaeffer Center
for Health Policy and Economics, one of the
nations premier health policy research
institutions. Dr. Goldman is the author of
over 150 articles and book chapters,
including publications in the most prestigious medical, economic, health policy, and
statistics journals. He is a health policy
advisor to the Congressional Budget Office,
18
Covered California (Californias insurance

exchange), and the Fred Hutchinson Cancer
Institute. He serves on several editorial
boards including Health Affairs and the
American Journal of Managed Care, and is
the founding editor of the Forum for Health
Economics and Policy. Dr. Goldmans work
has been featured in the New York Times,
Wall Street Journal, Washington Post,
Business Week, U.S. News and World Report,
The Economist, NBC Nightly News, CNN,
National Public Radio, and other media. In
2009, he was elected to the National
Academy of Sciences Institute of Medicine
in recognition of his professional achievement. He was the first recipient of the
MetLife Foundations Silver Scholar Award,
honoring his research on aging; the Eugene
Garfield Economic Impact Prize, recognizing outstanding research demonstrating
how medical research impacts the economy; the National Institute for Health Care
Management Research Foundation award
for excellence in health policy; and the
Alice S. Hersh New Investigator Award
recognizing contributions of a young
scholar to health services research. He is
also a founder and managing director of
Precision Health Economics, a consulting
firm to the health care industry. Dr. Goldman received his B.A. summa cum laude
from Cornell University and a Ph.D. in
Economics from Stanford University.
Claudia Gravekamp
Claudia Gravekamp,
PhD, is an Associate
Professor in the
Department of
Microbiology and
Immunology of the
Albert Einstein
College of Medicine
in New York, and a
member of the
Albert Einstein Cancer Center. She received
her PhD in 1988 in the field of Tumor
Immunology at the Erasmus University in
Rotterdam, The Netherlands. From 1987
to1993, she served as head of the Laboratory for Leptospirosis at the Royal Tropical
Institute in Amsterdam, The Netherlands. In
1993, she started as a Research Fellow in
Medicine at the Channing Laboratory of the
Brigham and Womens Hospital, Harvard
Medical School, and soon became an
Instructor in Medicine until 1998. There, she
developed vaccines against Group B
Streptococcus and gained expertise in the
design and development of gene-driven

vaccines. From 1998 to 2006, she was an
Associate Member in the Institute for Drug
Development of the Cancer Therapy and
Research Center and an Assistant Professor
at the University of Texas Health Science
Center, in San Antonio, where she began to
develop a program aimed at genetic
vaccines for breast cancer. From 2006-2008,
she was a Scientist at the California Pacific
Medical Center Research Institute in San
Francisco, continuing to develop novel
immunotherapeutic approaches to cancer
using attenuated Listeria monocytogenes as
a platform to deliver anti-cancer agents
selectively to the tumor microenvironment
at young and old age. She has been funded
by grants from the NIH, other grant agencies
and private industry since 1999, published
55 scientific articles, is a member of the
Editorial Board of Mechanisms of Ageing
and Development, and is ad-hoc reviewer
for various scientific journals.
Catalina Hoffman
Catalina Hoffman is
a leader in the
elderly sector for her
trajectory as
entrepreneur,
business woman
and Hoffmann
Methods creator.
She graduated with
a PDD from the IESE
Business School of Navarra University. She
has studied Occupational Therapy and is a
specialist in cognitive stimulation. The
Hoffmann Method offers an innovative
system of care and personalized attention
which takes into account the physical,
cognitive, psychological and social areas. It
has achieved improvements in the health
and quality of life of many people. It
includes a network of partners in the social,
health, scientific and technological sphere.
She is a member of the Board of Spain Startups Governing Council. She was named
President of SECOT in June 2013. She is
an associate and mentor of the European
Professional Womens Network. From
this network, she is godmother of Mapel
Project of Ayuda en Accin (NOG), aimed to
craftswoman entrepreneurs in Ecuador.
She also received national and international
recognitions including The Harvard
Business School Expansion Award for the
Speaker Biographies
Entrepreneurship. She was added to The
Top 100 Women Leaders in Spain 2012.
Plataforma Editorial published her first
book Emprender soando. The Prince of
Girona Foundation granted her the Award
of Business Woman 2013. The Association of
Young Entrepreneur of Madrid named her
the Young Entrepreneur of Madrid 2014.
In 2013, she created the Catalina Hoffmann
Holding Group, a group of companies
specialized in different areas of science,
health, health care, new technologies,
consulting, innovation and development
of new products and services. It includes
Vitalia, Hoffman Elderly,Hoffmann HealthCare Innovation and Catalina Hoffmann
Foundation.
Chris Hornsby
Chris academic
background is in
applied mathematics and epidemiology, his doctoral
research at University College London
was focused on
probabilistic models
of the multistage
development of cancer. Chris joined the
LifeRisks group at RMS in 2008 working
initially as lead developer of the RMS
Longevity Risk Model and subsequently
more broadly on insurance capital reserving and risk transfer applications in respect
of both life catastrophe and longevity.
Chris has played a key role, through the
provision of expert risk analysis, in the early
development of capital markets based
solutions for hedging longevity risk.
Jean Hbert
Jean Hbert Jean

Hbert completed
his PhD at the
University of
California, San
Francisco, under the
mentorship of Gail
Martin where he
studied cell-signaling
factors that regulate
some of the early steps in mammalian
development. For these studies, he used
embryonic stem cells and mouse genetics.
As a postdoctoral fellow in Susan McConnells lab at Stanford University, he then
focused his attention on how the neocortex,
the part of our brains that we use for our

highest cognitive and perceptual functions,
develops. Continuing along these interests,
he currently heads his own research lab at
the Albert Einstein College of Medicine
where his group has primarily undertaken
two lines of investigation.
approaches and stem cell-based therapies

to study skeletal muscle dysfunction
during aging and in age-associated muscle
diseases. The laboratory develops and
applies novel tools using a combination of
animal and stem cell models.
The first is understanding how a simple

sheet of neuroepithelial cells early in
embryogenesis develops into the adult
neocortex, seat of our consciousness.
Conditional genetic approaches in the
mouse, whereby candidate genes that
regulate neocortex formation are deleted
or overexpressed specifically in neural
precursor cells, comprise the central method
driving these studies.
Dr. Jerome is
Associate Professor
of Pathology,
Microbiology and
Immunology and
Associate Professor
of Cancer Biology at
Vanderbilt University. He is also
Co-Director of the
Cell Imaging Shared Resource at Vanderbilt.
Jay is a Past-president of the Microscopy
Society of America, the Co-Editor of a
textbook on confocal microscopy, and an
Editor for the journal Microscopy and
Microanalysis.
The second line of investigation aims to

establish ways of regenerating the principle
neurons of the adult cerebral cortex when
these neurons are lost due to trauma or
degeneration, including degeneration due
to aging. Since endogenous precursors do
not replace cortical neurons when they are
lost, two strategies are being developed:
manipulating these precursors with molecular genetic techniques to start generating
neurons and transplanting engineered
precursors that are programmed to disperse
in the cortex and differentiate into cortical
projection neurons.
Young Jang
Young Jang received

his Ph.D. in Biomedical Sciences (Cell
Biology) from
University of Texas in
2008, and completed
his postdoctoral
training from
Barshop Institute for
Longevity and Aging
Studies and the laboratory of Amy Wagers
at Harvard University and Harvard Stem
Cell Institute. In 2014, he was appointed as
an Assistant Professor in the School of
Applied Physiology and a faculty member
in the Parker H. Petit Institute for Bioengineering and Bioscience at Georgia Institute
of Technology.
The primary research focus of the Jang

laboratory is to understand the molecular and biochemical mechanisms of
age-related muscle loss and function. The
Jang laboratory applies bioengineering
W. Gray Jerome
Jays research focuses on intracellular lipid

metabolism and how disruption of normal
lipid metabolism contributes to disease. His
most recent studies investigate how lipids,
particularly cholesterol, affects lysosome
function and how alterations in lysosome
function feedback to influence lipid
metabolism. Lysosomes are key homeostatic organelles and lysosome dysfunction
is associated with a number of diseases
that become more prevalent with age. Dr.
Jerome has shown that cholesterol overload
inhibits lysosome function and disrupts cell
homeostasis, particularly in inflammatory
cells which can easily become overloaded
with cholesterol. His group has also shown
that lysosomal cholesterol-engorgement
shifts other aspects of cellular lipid balance
in ways that can push cells further into the
disease state.
Jeffrey Karp
Jeff Karp is an
Associate Professor
at Brigham and
Womens Hospital,
Harvard Medical
School, and is
Principal Faculty at
the Harvard Stem
Cell Institute and
affiliate faculty at MIT
through the Harvard-MIT Division of Health
Sciences and Technology. His research uses
19
Speaker Biographies
materials and biology to solve medical
problems with emphasis on nanoscale/
microscale materials and bio-inspiration. He
has published more than 100 peer-reviewed
papers and book chapters and has given over
130 national and international invited lectures
and has 50 issued or pending patents. Several
technologies that he has invented are
currently being translated into medical
products to improve the quality of life of
suffering patients.
In 2011 the Boston Business Journal recognized Dr. Karp as a Champion in Healthcare
Innovation and in 2013 the Institute for
Chemical Engineers (IChemE) awarded one
of his technologies the Most Innovative
Product of the Year. MITs Technology
Review Magazine (TR35) also recognized
Dr. Karp as being one of the top innovators
in the world under the age of 35. He has
received the Society for Biomaterials Young
Investigator Award and his work has been
selected as one of Popular Mechanics
Top 20 New Biotech Breakthroughs that
Will Change Medicine. Dr. Karp was also
elected in 2013 to the American Institute
for Medical and Biological Engineerings
College of Fellows and as a Kavli Fellow.
Dr. Karp is also an acclaimed mentor. He
was selected as the Outstanding Faculty
Undergraduate Mentor among all Faculty
at MIT and received the HST McMahon
Mentoring award for being the top mentor
among all faculty who mentor HarvardMIT students.
Michael Kope
Michael Kope is
President, Chief
Executive Officer,
and Co-founder of
the SENS Research
Foundation. Mr.
Kope received his
J.D. from the
University of
Michigan in 1990.
He has served as the University of
Michigans Intellectual Property Counsel;
as Director of Corporate Development for
Aviron, and for MedImmune, Inc.; and as
CEO and officer of a number of start-ups in
the biotechnology space. He specializes in
business development and consulting,
and is widely experienced with biotechnology organizations.
20
Mike has negotiated a broad range of

business acquisition and partnership
agreements, designed strategies for
technology protection and promotion in
many fields of research, and facilitated a
number of successful startups.
Daniel Kraft
Daniel Kraft is a
Stanford and
Harvard trained
physician-scientist,
inventor, entrepreneur and innovator.
Dr. Kraft has over 20
years of experience
in clinical practice,
biomedical research
and healthcare innovation. Daniel chairs
the Medicine track for Singularity University and is Founding Executive Director for
FutureMed (now called Exponential
Medicine), a program which explores
convergent, exponentially developing
technologies and their potential in
biomedicine and healthcare.
Following undergraduate degrees at
Brown University and medical school at
Stanford, Dr. Kraft was board certified in
the Harvard combined Internal Medicine
and Pediatrics residency program at the
Massachusetts General Hospital and
Boston Childrens Hospital. He went on
to complete Stanford fellowships in
hematology/oncology & bone marrow
transplantation, and to conduct extensive
research in stem cell biology and
regenerative medicine. He has multiple
scientific publications (including in the
journals Nature and Science) and medical
device, immunology and stem cell related
patents through faculty positions with
Stanford University School of Medicine
and as clinical faculty for the pediatric
bone marrow transplantation service at
University of California San Francisco.
Dr. Kraft recently founded Bioniq Health,
focused on enabling connected, data
driven, and integrated personalized
medicine. He is also the inventor of the
MarrowMiner, an FDA approved device
for the minimally invasive harvest of
bone marrow, and founded RegenMed
Systems, a company developing technologies to enable adult stem cell based
regenerative therapies.
Neil Littman
Neil Littman is the

Business Development Officer at the
California Institute
for Regenerative
Medicine. Mr.
Littman is responsible for facilitating
opportunities for
outside investment
in stem cell research in California by
biopharma companies, investors, and
disease foundations.
Prior to joining CIRM in 2012, Mr. Littman
was a Senior Associate in the Merchant
Banking Group at Burrill & Company, a
diversified global financial services firm
focused on the life sciences industry based
in San Francisco. While at Burrill & Company,
Mr. Littmans responsibilities included both
strategic advisory and capital raises for
biopharma companies throughout the U.S.
and internationally.
Mr. Littmans strategic advisory experience
includes buy-side and sell-side M&A, as well
as in-licensing and out-licensing of both
development stage and commercial products. Prior to joining Burrill & Company in
2009, Mr. Littman worked in the Healthcare
Investment Banking group at Thomas Weisel
Partners where he focused on strategic
advisory and public and private financings.
Prior to Thomas Weisel Partners, Mr. Littman
worked in the Healthcare Investment
Banking group at Deutsche Bank Securities.
Mr. Littman received a Master of Science
in Biotechnology with a concentration in
Biotechnology Enterprise from The Johns
Hopkins University, and a Bachelor of Arts in
Molecular, Cellular and Development Biology
from the University of Colorado Boulder.
Jeanne Loring
Jeanne Loring, Ph.D.,

is a Professor and
the founding
Director of the
Center for Regenerative Medicine at The
Scripps Research
Institute in La Jolla.
Her research team
focuses on largescale analysis of genomics and epigenetics
of human pluripotent stem cells (hPSCs) and
Speaker Biographies
their derivatives, in order to ensure the
quality and safety of these cells for clinical
use. The teams translational projects include
development of cell therapies for Parkinsons disease, multiple sclerosis, and
Alzheimer disease, and epigenetic modeling
of autism. The team is also producing an
ethnically diverse library of iPSC (induced
pluripotent stem cell) lines for use in
pharmaceutical screening. In addition, her
lab is developing a zoo of induced
pluripotent stem cells from endangered
species to aid in their conservation.
Dr. Loring is committed to educating both
scientists and the public. She has trained
more than 400 scientists over the last 10
years in intensive laboratory courses in
human ES and iPSC biology, and is author
of a comprehensive laboratory manual on
human pluripotent stem cells (Human
Stem Cell Manual: a Laboratory Guide, in
second edition, 2012). She is frequently
quoted in major newspapers, and gives
numerous public lectures and interviews
to inform the public about biological and
societal issues associated with stem cell
research, including the ethics of stem
cell generation and clinical use, the legal
implications of stem cell patents, and
public education about the dangers of
unregulated stem cell treatments (stem
cell tourism). Dr. Loring serves on both
bioethics and scientific advisory boards.
Linda Marban
Linda Marban is
currently CEO,
President and
Director of Caprico
Therapeutics. She
combines her
background in
research with her
business experience
to lead Capricor and
create a path to commercialization for its
novel stem-cell cardiac therapies. Dr.
Marban was the lead negotiator in procuring the license agreements that are the
foundation of Capricors intellectual
property portfolio. Under her direction as
Chief Executive Officer, Capricor secured
approximately $27.0 million in nondilutive
grants and a loan award which funds
Capricors R&D programs and clinical trials
involving its CAP-1002 product. Dr. Marbans
deep knowledge of the cardiac space in
particular, allows her to provide unique
direction for the companys development

and growth. From 2003 to 2009, Dr. Marban
was with Excigen, Inc., a biotechnology
start-up company, where she was responsible for business development, operations,
pre-clinical research, and supervising the
development of gene therapy products in a
joint development agreement with Genzyme Corp. While at Excigen, she also
negotiated a joint development and
sublicense agreement with Medtronic Corp.
utilizing Excigens technology and supervised the building of a lab in which the work
was to be performed.
Dr . Marban began her career in academic
science at the Cleveland Clinic Foundation
working on the biophysical properties of
cardiac muscle. She moved to a postdoctoral fellowship at Johns Hopkins University
and advanced to the rank of Research
Assistant Professor in the Department of
Pediatrics, continuing her work on the
mechanism of contractile dysfunction in
heart failure. Dr. Marban earned a Ph.D.
from Case Western Reserve University in
cardiac physiology.
Andrew Martello
Andrew Martello is
co-founder & CEO of
Spoonful of Sugar
(SoS). He leads an
expert team
developing
academically-led
adherence consultancy and evidence-based
adherence solutions to global healthcare
providers and the pharmaceutical industry.
SoS is a University College London spinout

company that applies the learnings of a
15-year research program in behavioral
medicine, specifically, how patients engage
with long-term illnesses and treatment.
Over the past five years, Andrew has
been directly involved in the planning
and implementation of multi-country
adherence and patient support programs
utilizing the latest research into illness and
medicines-related behavior. As part of this
work, Andrew has led the development of
proprietary software designed to diagnose
and treat both perceptual and practical
barriers to optimal adherence at an
individual patient level.
Passionate about the role of digital

technology in changing health behaviors,
Andrews main interest is the role of
personalized medicine, from both a clinical
and psychological perspective and its real
world application.
Prior to founding SoS, Andrew spent over
ten years working for and consulting with
the pharmaceutical industry, predominantly
in HIV medicine.
Much of his work in this field focused on
the development of strategies supporting a
greater understanding of the patients perspective throughout the drug development
and product lifestyle pathway. This included
the development of novel formulations and
devices, packaging and support services to
optimize the use of medicines.
This work not only focused on the developed world but also included innovative
strategies to widen access to medicines
throughout the developing world.
Andrews previous assignments have been
with GlaxoSmithKline, Abbott Laboratories,
Novartis and Sandoz Biopharmaceuticals.
Stephen Minger
Dr. Stephen Minger

received his PhD in
Pathology (Neurosciences) in 1992
from the Albert
Einstein College of
Medicine in New
York City. After
post-doctoral work
in central nervous
system gene therapy, neural transplantation
and neural stem cell biology, he was
appointed a Lecturer in Biomolecular
Sciences at Kings College London in 1998.
He was appointed a Senior Lecturer in Stem
Cell Biology in 2005 and was the Director of
the Stem Cell Biology Laboratory from 2002
until joining GE Healthcare in 2009.
Over the past 20 years, Stephens research
group has been at the forefront of human
stem cell research. In 2002, they were
awarded one of the first two licenses
granted by the UK Human Fertilisation and
Embryology Authority for the derivation
of human embryonic stem (hES) cells and
his group was the first to deposit a hES cell
line into the UK Stem Cell Bank. Stephens
21
Speaker Biographies
was also one of the first two groups in the
UK to be granted a research license by
the HFEA in 2008 to pursue Somatic Cell
Nuclear Transfer (SCNT) to generate hybrid
human embryos for fundamental research
into genetic forms of neurodegenerative
conditions. He was activity involved with
the UK Department of Health and in the
consultation that led to the passage of
the Human Embryo Bill of 2009 and the
inclusion of new forms of animal-human
embryos within primary legislation.
In the summer of 2013, Stephen was
appointed Chief Scientist for Cellular
Sciences, GE Healthcare Life Sciences, and
is now responsible for long-term global
research strategy for technology development in cell therapy, regenerative medicine,
cellular technologies, in vivo diagnostic
imaging and molecular pathology/personalized medicine.
Peter Nakada
Peter Nakada leads

the RMS Capital
Markets and
LifeRisks groups.
After joining the
company in 2005,
he formed the RMS
Capital Markets
group to provide an
infrastructure for
capital markets participants to understand
catastrophe risk. He focuses on taking the
companys catastrophe risk expertise into
adjacent markets and leads the RMS
LifeRisks team to provide excess mortality
and longevity risk analytics to life insurers
and capital markets investors.
Nakada began his career in financial services
as a general account fixed income portfolio
manager for Prudential Insurance Company.
Prior to joining RMS, Nakada was a partner
at Oliver, Wyman & Company, where he
specialized in advising banks and insurers
on aspects of risk, capital, and shareholder
value. In 2000, Nakada co-founded ERisk,
a spinoff from Oliver, Wyman & Company,
which provides software-as-a-service for
enterprise risk management and economic
capital quantification.
Nakada has co-authored many articles on
topics related to risk, capital, and shareholder value, as well as the securitization of
catastrophic risk. His articles include Risk,
22
Capital & Value Measurement in Financial

Institutions Part I: The Debtholders
Perspective (1998),P&C RAROC: A Catalyst
for Improved Capital Management in
the Property and Casualty Insurance
Industry (1999), Understanding Longevity
Risk:Insights from Structural Cause-of-Improvement Models (2012) and Quantifying
the Mortality-Longevity Offset(2013).
Nakada holds a bachelors degree in
engineering sciences from Harvard College
and a masters degree in engineering
management from Stanford University. He
earned the Chartered Financial Analyst
designation in 1990.
Edward James Olmos
Edward James
Olmos (Axford) has
achieved extraordinary success as an
actor, producer and
humanitarian. The
Tony, Emmy and
Academy Award
Nominated actor, is
probably best
known to young audiences for his work on
television series Battlestar Galatica as
Admiral William Adama. Although the
series kept the actor busy during its run
from 2003 through 2009, it didnt stop him
from directing the HBO movie Walkout
in 2007, for which he earned a DGA
Nomination in the Outstanding Directorial
Achievement in Movies for Television
category.
Olmos earned two Golden Globe and
Emmy Award nominations, resulting in
a win from each. In 1988, he received an
Academy Award nomination for Best Actor
for his starring role in Stand and Deliver
and won the Golden Globe for his portrayal
of Jaime Escalante in Stand and Deliver.
Olmos career in entertainment spans over
30 years. In that time he created a signature style and aesthetic that he applies to
every artist endeavor. His dedication to his
craft has brought him worldwide attention.
Olmos went on to appear in the films
Wolfen, Blade Runner, and the Ballad of
Gregorio Cortez before starring in his
biggest role to date, that of Lieutenant
Martin Castillo in the iconic 80s television
series Miami Vice.
He directed and starred in his first motion

picture, American Me, in 1992.
Olmos passion for the arts grows every
year, but he never forgets to give back to
the communities that support him with
their dedication.
He is an international advocate, spokesman,
and humanitarian working with organizations such as Thank You Ocean, Project
Hope Foundation, Childrens Hospital of
Los Angeles, The Boys and Girls Club of
America, The River Keepers, Dr. Andros
Diabetic Foot Global Conference and he
speaks up to 150 times a year in schools,
universities, and corporations.
Jim ONeill
Jim ONeill is partner

and chief operating
officer at Mithril, a
growth fund for
transformative and
durable technology
companies in fields
such as cybersecurity; next
generation finance;
medical robotics; rail integration; enterprise cloud services; 3D seismic technology; and data integration, visualization,
and analysis. Mithril invests with conviction and helps teams successfully navigate
high-growth periods.
Before helping to launch Mithril, Jim was

a managing director of Clarium, a global
macro investment fund. He also ran the Thiel
Foundation and co-founded the 20 Under
20 Thiel Fellowship and Breakout Labs.
Previously, as the principal associate
deputy secretary of health and human
services, Jim helped manage an agency
whose 67,000 employees regulate more
than 25% of the U.S. economy. His main
areas of policy and program responsibility
included the Food and Drug Administration, the National Institutes of Health, the
Centers for Disease Control and Prevention,
security, intelligence, preparedness, and
health diplomacy. He also made investments in drug, vaccine, and diagnostic
research on the steering committee of
the $200 million Biomedical Advanced
Research and Development Authority.
Speaker Biographies
Brock Reeve
Brock Reeve is
Executive Director
of the Harvard Stem
Cell Institute. In
partnership with the
Faculty Directors, he
has overall responsibility for the
operations and
strategy of the
Institute whose mission is to use stem cells,
both as tools and as therapies, to understand and treat the root causes of leading
degenerative diseases.
HSCI is comprised of the schools of Harvard
University and all its affiliated hospitals and
research institutions. Under the leadership
of the Executive Committee, HSCI invests in
scientific research and its faculty has grown
to include over 300 Principal and Affiliated
members. The Institute is engaged with
several leading pharmaceutical companies
and foundations in joint research projects
and its faculty have founded several stem
cell-related startup companies and serve on
leading Scientific Advisory Boards.
Brock came to this role from the commercial
sector with extensive experience in both
management consulting and operations for
technology-based companies, with a focus
on life sciences. Brock received a BA and
MPhil from Yale University and an MBA from
Harvard Business School.
Camillo Ricordi
Camillo Ricordi is
Professor and
Director of the
Diabetes Research
Institute (DRI; www.
diabetesresearch.
org ) and the Cell
Transplant Program
Miami.
Dr. Ricordi and collaborators developed

the method for large scale production of
human pancreatic islets, and he led the
team that performed the first series of
successful clinical islet allotransplants to
reverse diabetes. The procedure is now
used by laboratories performing clinical
islet transplants worldwide. Ricordi was
president of the Cell Transplant Society,
on the NIH-NIAID Expert Panel on clinical
approaches for tolerance induction, on

the FDA Biologic Response Modifiers
Advisory Committee and on the NIHNIDDK Strategic Planning Committee.
Ricordi is currently serving as Chairperson
of the NIH funded Clinical Islet Transplantation (CIT) Consortium, which standardized
cell manufacturing protocols in North
America and Europe and just completed
the first multicenter FDA Phase III trial for
what could become the first biologically
active cell product approved in the US by
the FDA.
Ricordi has received numerous honors and
awards and was also Knighted by the President of the Republic of Italy. He is currently
serving on the editorial boards of CellR4
(Editor-in-Chief; www.cellr4.org) and Cell
Transplantation (Co-Editor-in-Chief ). In
2013 he was appointed President of the
Ri.MED Foundation by the Italian Prime
Minister (http://www.fondazionerimed.eu),
one of the largest European investments in
Biomedical Research, Biotechnologies and
Regenerative Medicine. Ricordi also serves
as President of The Cure Alliance (www.
thecurealliance.org) and Chairman of the
Diabetes Research Institute Federation
(www.diabetesresearch.org). He has
authored over 700 scientific publications
and 19 awarded patents.
David Schaffer
David Schaffer is a
Professor of
Chemical and
Biomolecular
Engineering,
Bioengineering, and
Neuroscience at
University of
California, Berkeley,
where he also
serves as the Director of the Berkeley Stem
Cell Center. He graduated from Stanford
University with a B.S. degree in Chemical
Engineering in 1993. Afterward, he
attended Massachusetts Institute of
Technology and earned his Ph.D. also in
Chemical Engineering in 1998. Finally, he
did a postdoctoral fellowship in the
laboratory of Fred Gage at the Salk Institute
for Biological Studies in La Jolla, CA before
moving to UC Berkeley in 1999.
neuroregeneration, work that includes

novel approaches for molecular engineering and evolution of new viral vectors as
well as new technologies to investigate
and control stem cell fate decisions.
David Schaffer has received an NSF
CAREER Award, Office of Naval Research
Young Investigator Award, Whitaker
Foundation Young Investigator Award, and
was named a Technology Review Top 100
Innovator. He was also awarded the Biomedical Engineering Society Rita Shaffer
Young Investigator Award in 2000, the
American Chemical Society BIOT Division
Young Investigator Award in 2006, and
was inducted into the College of Fellows
of the American Institute of Medical and
Biological Engineering in 2010.
Dale Schenk
Dr. Dale Schenk,

Chief Executive
Officer of Prothena,
plc, was previously
Chief Scientific
Officer and Executive Vice President at
Elan Pharmaceuticals where he
provided the
leadership and scientific direction for Elans
research and development programs. Prior
to joining Elan, Dr. Schenk was a founding
scientist of Athena Neurosciences, which
was acquired by Elan Pharmaceuticals.
Dr . Schenk has pioneered the immunotherapeutic approaches for the treatment
of amyloidosis, as exemplified for Alzheimers disease, Parkinsons disease and light
chain (AL) Amyloidosis. Dr. Schenks work
in this area, as well as in early detection,
testing and other pathways to these
diseases, has led specifically to the most
advanced potential treatment approach
for Alzheimers disease. Clinical trials are
also currently underway for AL amyloidosis and Parkinons disease that utilize
immunotherapy.
Dr . Schenk earned his BA and PhD in
Pharmacology and Physiology from the
University of California, San Diego.
At Berkeley, Dr. Schaffer applies

engineering principles to enhance stem
cell and gene therapy approaches for
23
Speaker Biographies
Michael Sherratt
Following a PhD
and postdoctoral
positions with
Professor Cay Kielty
Manchester,
Michael was
awarded an AgeUK
Fellowship and
Senior Fellowship.
He is currently a Lecturer in Molecular
Biochemistry at the University of Manchester and director of the BioAFM (atomic
force microscopy) Facility at the same
institution. For the past four years he has
served as treasurer of the British Society for
Research on Ageing and his main research
interests are in the effects of ageing on
tissue extracellular matrix structure and
mechanical function.
Using biochemical, ultra-structural, bioinformatic and micro-mechanical approaches,
Michaels work suggests that: i) elastic
fibre associated proteins (which are highly
enriched in Cys, Trp and Tyr amino acid
residues) may be differentially susceptible
to UV-radiation and oxidation in ageing
tissues and ii) the effects of ageing on tissue
mechanical properties are localized in large
arteries such as the aorta.
In collaboration with colleagues in the
Manchester X-ray Imaging Facility he is now
developing new imaging methodologies
to characterize the effects of intra-luminal
pressure on the 3D structure of young and
aged arteries.
Bernard Siegel
Bernard Siegel, J.D.,

is the founder and
Executive Director
of Genetics Policy
Institute (GPI), a
nonprofit organization with offices in
Palm Beach, Florida;
Silicon Valley,
California and
Washington, D.C. He founded and co-chairs
the annual World Stem Cell Summit,
founded and serves editor-in-chief of the
peer-reviewed World Stem Cell Report and
is the editor of the 360 Stem Cell & Regenerative Medicine weekly newsletter. He
founded and is the spokesperson for the
Stem Cell Action Coalition, a 100+ member
24
international alliance of nonprofits and

research institutions leading the global
Pro-Cures Movement.
In 2002, he filed the first court case relating
to reproductive cloning and is widely
credited for debunking the claim of the
group claiming that they cloned the first
baby. He also played a pivotal leadership
role in galvanizing a global movement that
successfully lobbied the United Nations to
reject a treaty that called for a prohibition
of nuclear transfer, or therapeutic cloning.
As a recognized policy expert on stem cell
research, regenerative medicine and cloning,
he works with leading scientists and patient
advocates, raising public awareness and
educating lawmakers, the media and public
on stem cells and regenerative medicine. He
is a frequent panelist and keynote speaker
on the subject of stem cells, public policy
and patient advocacy.
Eric Siemers
Eric Siemers, M.D. is

the Senior Medical
Director of the
Alzheimers Disease
Global Development Team at Eli
Lilly and Company.
He earned his MD
with highest
distinction from the
Indiana University School of Medicine in
1982. After an internship in the Department
of Internal Medicine at the Indiana University School of Medicine, he completed his
residency in the Department of Neurology
in 1986. Prior to joining Lilly, he founded
and headed the Indiana University Movement Disorder Clinic; his previous research
included investigations of Parkinsons
disease and Huntingtons disease, and he
established one of the first centers for
surgical PD treatments in the US.
Dr . Siemers currently directs late stage
clinical research efforts at Lilly concerning
investigational treatments for Alzheimers
disease, and is more broadly involved
with other neurological indications such
as Parkinsons disease. Major research
interests include the use of biomarkers
in investigational drug research and the
development of trial designs that broadly
characterize the effects of investigational
drugs on chronic diseases.
Dr . Siemers is a founding member and

current Chair of the Alzheimers Association
Research Roundtable. He is a member of
the Steering Committee for the Alzheimers
Disease Neuroimaging Initiative (ADNI). He
served as the chair of the Industry Scientific
Advisory Board for ADNI in 2007. Dr. Siemers
is a current member of the New York
Academy of Sciences Alzheimers Disease
Leadership Counsel. He participated as a
member of the NIA working group that
proposed criteria for preclinical Alzheimers
disease in 2011. He is a past member of the
Board of Directors of the American Society
of Experimental Neurotherapeutics.
Einar M. Sigurdsson
Einar M. Sigurdsson,
Ph.D. is a tenured
Associate Professor
of Neuroscience and
Physiology, and
Psychiatry at New
York University
School of Medicine.
A native of Iceland,
he received a
masters degree in Pharmacy from the
University of Iceland, and a Ph.D. in Pharmacology from Loyola University Chicago
Medical Center. He subsequently obtained
postdoctoral training at New York University
School of Medicine.
His current research focuses on pathogenesis, therapy and diagnosis for age-related
protein conformational disorders, in
particular Alzheimers disease.
His honors include a Zenith Fellows Award
and the Margaret M. Cahn Research Award
from the Alzheimers Association, and the
Irma T. Hirschl Career Scientist Award. He is
presently serving as a standing member on
an NIH study section.
Dr. Sigurdsson and his collaborators pioneered the use of modified A derivatives
as potential immunotherapy for Alzheimers
disease. Furthermore, they showed for the
first time that active and passive immunization as well as chelators delayed the onset
of prion disease in mice, with follow up
immunization studies leading to prevention
of clinical symptoms in mice.
On the diagnostic front, Dr. Sigurdsson
and colleagues published the initial report
on detection of amyloid plaques in living
Speaker Biographies
mouse brains by magnetic resonance imaging. Lately, he has pioneered the approach
to harness the immune system to target
pathological tau protein in Alzheimers
disease and other tauopathies.
Evan Y. Snyder
Dr. Snyder earned

his M.D. and his Ph.D.
in neuroscience
from the University
of Pennsylvania in
1980. He completed
residencies in
pediatrics and
neurology at
Childrens Hospital-Boston, Harvard Medical School and
postdoctoral research at Harvard Medical
School. In 1992, Dr. Snyder was appointed an
instructor in neurology at Harvard Medical
School and was promoted to assistant
professor in 1996.
He is regarded as one of the fathers of
the stem cell field, having identified over
2 decades ago that cells that came to be
called stem cells were a source of neural
plasticity. He was the first to demonstrate
that non-hematopoietic stem cells could
mediate cell and gene replacement, home
to injury, and perform protective, trophic,
pro-regenerative, and anti-inflammatory
actions. He was the first to isolate human
neural stem cells.
In 2003, after 23 years at Harvard, Dr. Snyder
was recruited to Sanford Burnham Medical
Research Institute as professor and director
of the Stem Cells and Regeneration program.
Michael D. West
Michael D. West,
Ph.D. became Chief
Executive Officer of
Biotime during
October 2007, and
has served on the
Board of Directors
since 2002. Prior to
becoming Chief
Executive Officer, Dr.
West served as Chief Executive Officer,
President, and Chief Scientific Officer of
Advanced Cell Technology, Inc., a company
engaged in developing human stem cell
technology for use in regenerative medicine.
Dr . West also founded Geron Corporation

of Menlo Park, California, and from 1990 to
1998 he was a Director and Vice-President,
where he initiated and managed programs
in telomerase diagnostics, oligonucleotide-based telomerase inhibition as
anti-tumor therapy, and the cloning and
use of telomerase in telomerase-mediated
therapy wherein telomerase is utilized to
immortalize human cells. From 1995 to 1998
he organized and managed the research
between Geron and its academic collaborators James Thomson and John Gearhart that
led to the first isolation of human embryonic
stem and human embryonic germ cells.
Dr . West received a B.S. Degree from
Rensselaer Polytechnic Institute in 1976,
an M.S. Degree in Biology from Andrews
University in 1982, and a Ph.D. from Baylor
College of Medicine in 1989 concentrating
on the biology of cellular aging.
Claude Wischik
Claude Wischik is
Professor of Old Age
Psychiatry at the
University of
Aberdeen and
Executive Chairman
of TauRx Therapeutics. He studied
medicine in
Australia, then PhD
and post-doctoral research at the MRC
Laboratory of Cambridge, UK. He also
completed psychiatric training in
Cambridge.
James Yoo
Dr. Yoo is a surgeon

and researcher. He is
currently a Professor,
Associate Director
and Chief Scientific
Officer at the Wake
Forest Institute for
Regenerative
Medicine. Dr. Yoos
research efforts
have been directed toward the clinical
translation of tissue engineering techno
logies and cell-based therapies. Dr. Yoos
background in cell biology and medicine
has facilitated the transfer of several
cell-based technologies from the bench-top
to the bedside.
A few notable examples of successful clinical

translation include the bladder, urethra,
vagina and muscle cell therapy for incontinence. Other technologies that are being
developed for translation include therapies
for renal, liver and cardiovascular pathologies, skin bioprinting and skin expander for
the treatment of burn patients.
Dr. Yoo has served in many institutional,
national and international committees
and advisory boards. He has successfully
organized and directed many scientific
meetings and symposia, and managed
numerous multi-institutional and international collaborative research projects and
programs. He has actively contributed to
the scientific community through publication, meeting presentations and lectures
internationally.
During his PhD he discovered that the

neurofibrillary tangle is composed of the
microtubule associated protein Tau. He also
discovered that they could be dissolved
by diaminophenothiazines. He established
a team which developed in vitro and in
vivo systems to establish plausibility of
developing Tau Aggregation Inhibitor (TAI)
therapy for AD.
He cofounded TauRx Therapeutics to
develop diagnostics and therapeutics for
AD based on the TAI approach. In the first
ever TAI phase 2 trial, TauRx demonstrated
the feasibility of arresting disease progression over 12 months. TauRx is currently
conducting a global phase 3 trial of its lead
compound in approximately 1,500 subjects
in 22 countries.
25
Sierra Sciences shares the SENS

Research Foundations mission of
extending the human lifespan and
pursuing healthy longevity.
Mountain View, CA
Congratulations SRF, on your

innagural U.S. Conference!
Cure Aging or Die Trying
www.SierraSci.com
Look and Feel Younger

with a Complimentary Life Extension Foundation Membership
$37.50 VALUE
Did you know that you can feel
healthier, avoid disease, extend
your life, and maybe even save
it? If you or your loved ones want
to achieve better health, join the
Life Extension Foundation
the worlds largest non-profit
organization dedicated to
ongoing research on anti-aging
and optimal health.
Life Extension offers you the most

advanced life-extending therapies
in the world as they are developed.
New Members receive:
At the forefront of scientific

research, Life Extension offers
information on:
Heart Disease, Diabetes, Cancer,
and Other Illnesses
Anti-Aging and Hormone
Replacement Therapies
Age-Related Memory Loss
Vitamins, Minerals, Antioxidants,

and Other Supplements
And Much More
A 6-month subscription ($29.94

newsstand value) to the informative
Life Extension Magazine, filled with
medical research, news reports, abstracts,
updates, and more. (Plus, youll have the
option to receive the Life Extension Update
conveniently delivered via e-mail, featuring
timely articles to help you stay fit for life.)
Discounts of 25% to 50% on all Life Extension Foundation
Buyers Club products. Plus, special sales during the year
offer even greater discounts on these extraordinary products.
Direct access toll-free to
a knowledgeable team of
Health Advisors who can
help you personalize a
unique anti-aging program
and provide you with
answers about health
concerns and supplements.
Life Extension Annual
Directory a comprehensive listing of products,
many available only from
Life Extension.
o YES! I want to join the Life Extension Foundation for 6 months (new members only) at no charge to me.
I understand there is no obligation to renew, and my satisfaction is guaranteed.
Name
Item code: MEMBFREE6M
Phone
(please print)
Address
City, State, Zip
E-mail
o Yes, I want to receive the weekly FREE Life Extension Update by e-mail. I can unsubscribe at any time.
Life Extension Foundation
P.O. Box 407198 Fort Lauderdale, FL 33340
Or Call Toll Free 1-800-544-4440 Fax: 1-866-728-1050
Discount Code: AVG404A
656.27A 0814
Mail To:
EXCLUSIVE
OFFER
for SENS
attendees:
FREE 12 Month Subscription to the

AGING MATTERS MAGAZINE worth $48.00
The Aging Matters Magazine is published by the IAS Group. Since 1991 the
IAS Group has been making the latest information and products available
worldwide, we showcase the very best and our private club magazine is
read by over 50,000 readers 6 times a year.
The Aging Matters Magazine has articles from leading
professionals, a Q&A by the renowned smart drug pioneer
Dr. Ward Dean and a full run down of the
250 essential products for the
preventative and regenerative
health enthusiast.
To claim your free subscription, simply sign up for an account at:

www.antiaging-systems.com/subscribe
Tel: +44 208 123 2106 Web: www.antiaging-systems.com
The leading peer-reviewed

journal publishing
cutting-edge research on
rejuvenation therapies in
the laboratory and clinic
Rejuvenation
Research
Editor-in-Chief
Aubrey D.N.J. de Grey
WF
WVI
Sign up for TOC Alerts!

www.liebertpub.com/rej
OF
W ORLD F EDERATION (WF) &

W ORLD V IRTUAL I NSTITUTE (WVI)
P RE V E NT I V E & R EG EN ER A TI V E M ED I C I N E
The Official Journal of PYRAMED: World Federation & World

Virtual Institute of Preventive & Regenerative Medicine
The Official Journal of the European Society

of Preventive, Regenerative and Anti-Aging Medicine (ESAAM)
Save the Date
SENS7 Conference
September 3 to 7, 2015
Queens College
Cambridge, England
Poster Abstracts
1. THE TARGETED DELIVERY OF CYTOKINES BY
AUTOLOGOUS ERYTHROCYTE GHOSTS
Authors: Berikkhanova K, Gulyayev A, Shulgau Z, Ibrasheva D,
Bokebaev Z, Mussin N, Nurgozhin T, Askarova S, Zhumadilov Z
Presenter Institutions: PI Center for Life Sciences; JSC Nazarbayev
University
Targeted delivery of cytokines by autologous erythrocyte ghosts
may create high concentrations of cytokines in blood plasma or
in certain body tissues for a long period of time. This is highly
important in treatment of surgical patients with purulent diseases.
Activity of various cytokines has been studied and the results for
interleukin IL-1 and recombinant human angiogenin activity
are presented. The goal of this research was to assess the activity
of IL-1 and recombinant human angiogenin encapsulated into
erythrocyte ghosts compared to intravenously injected free form
of both cytokines.
Cytokines were encapsulated by the method of hypotonic hemolysis. The experiments were performed using albino rats with
mass of 200.0-220.0 g (n = 28). Both cytokines were used in two
dosage forms: encapsulated in autologous erythrocyte ghosts
and standard free form. Animals were randomly divided into four
groups, and each group received a different kind of intravenous
injection of a certain cytokine via the tail vein. Group A received
500 g of free IL-1, group B received an injection of erythrocyte
ghosts loaded with 500 g of IL-1. Group C received 4000 pg of
free angiogenin, group D received an injection of erythrocyte
ghosts loaded with 4000 pg of angiogenin. For all groups serum
samples were collected at 15, 30, 60, 180, 540, 720, and 1440 minutes after IV injections. Homogenates of liver, spleen, lung, heart,
kidney, and adipose tissue were obtained 24 hours after injections.
Concentrations of the tested substances in the collected organs
and blood plasma were measured by ELISA. Modeling was performed using Borgia 1.03 software.
We observed an increased half-life period (T1/2) for encapsulated
IL-1 and angiogenin compared to the control. After introduction
of free IL-1 the half-life period was equal to about one hour,
when administration of loaded erythrocyte ghosts allowed the
half-life period to increase by more than 15 fold (1043.40 137.92
min). After introduction of free angiogenin the half-life period was
equal to about 32 min., when administration of loaded erythrocyte ghosts allowed the half-life period to increase by more than
9 fold (296,3 31.6 min). The increase of the residence time of
cytokines in the body when administered in the form of loaded
erythrocyte ghosts can be explained by reduction of elimination
constant (Cel) and clearance (CLel). High levels of IL-1 and angiogenin activity remained in the blood throughout 24 hours. We
also observed an increased concentration of IL-1 and angiogenin
in liver, and spleen during at least 24 hours; when administered in
free form, IL-1 and angiogenin disappeared from these organs
within 6 hours.
Erythrocyte ghosts provide prolong action of IL-1 and angiogenin in the body by increasing the half-life period, reducing the
clearance and elimination time, as well as due to the deposition of
IL-1 and angiogenin in liver and spleen. These data suggest that
erythrocyte ghosts are effective drug carriers for targeted delivery

of cytokines and can potentially provide a significant therapeutic
effect maintaining the stable level of cytokines in the blood and
its deposition to liver and spleen.
2. BIOLOGICAL ACTIVITIES OF AQUEOUS EXTRACT OF

INDIAN SANDALWOOD
Author: Fatima S
Presenter Institution: Jamia Millia Islamia
Santalum album, commonly known as sandalwood, is used
traditionally in India. It is an evergreen and hemi-parasitic tree
and has a long history in Indian religious rituals and traditional
Chinese medicine. Due to its wide application in cosmetics and
therapeutics, we have done this study to explore the possibility of
using aqueous extract of S. album as antibacterial and antioxidant
agent. The S. album extract was prepared in distilled water. The
activity of aqueous extract was evaluated against eight bacterial
pathogens including two strains of Escherichia coli, one each of
Klebsiella pneumoniae, Staphylococcus aureus, Bacillus subtilis,
Pseudomonas aeruginosa, Aeromonas species, and Klebsiella
oxytoca. The anti-oxidant activity was analyzed by two of the
most common radical scavenging assays, FRAP (ferric reducing
antioxidant power) and DPPH (1,1- diphenyl-2-picrylhydrazyl).
Results showed that S. album had the strongest inhibitory activity
against S. aureus (MTCC 902) i.e. 87% whereas, it showed no
inhibition against E.coli (ATCC 25922) and B. subtilis (MTCC736).
The S. album extract showed DPPH radical scavenging activity in a
concentrationdependent manner with maximum scavenging of
64% in presence of 500 l of aqueous extract. The FRAP assay also
proved antioxidant potential of S. album with the highest value of
0.628mM at 200l of aqueous extract.
3. NON-ENZYMATIC GLYCATION AND ASSOCIATED

DEFENSE MECHANISM: UNIVERSAL DETERMINANTS OF
VIABILITY AND SENESCENCE IN ALL FORMS OF LIFE
Authors: Szwergold B, Miller C
Presenter Institution: Deglycation Research
Non-enzymatic glycation reactions (a.k.a. Maillard reactions)
are major contributors to senescence and have been a focus of
intensive studies in connection to diabetic complications. It was
noted only recently that Maillard reactions are a challenge to
all organisms and consequently, defense mechanisms against
non-enzymatic glycation (anti-Maillard defenses) are a ubiquitous feature of life.
We have contributed to this growing awareness by explicitly
raising the issue of anti-Maillard defenses in organisms as diverse
as hyperthermophilic archaea and birds. We have proposed
some concrete and testable hypotheses, but even more importantly, we have, for the first time, explicitly formulated and
published such questions.
Most recently we have directed out attention to autrophic
organisms (plants) in which Maillard reactions have not been
studied much. Notable exceptions to this neglect are two
33
Poster Abstracts
recent papers that present unequivocal evidence of Maillard
reactions in plants. Significantly, these reactions appear to be
stimulated by photosynthesis.
These studies, however, neglected to probe the most important
Maillard-related compound in plants; ribulose-1,5-bisphosphate
(RuBP). This indispensable photosynthetic intermediate is found
in high concentrations in all chloroplasts and is an extremely
potent glycating agent.
We postulate that RuBP-mediated glycation and defenses against
it are important factors in determining senescence of plants and
that understanding these processes may be of value in devising
anti-Maillard therapies for humans.
4. BIRDS AS A PATHOLOGY-FREE MODEL OF TYPE 2

DIABETES. THREE CONTRIBUTING FACTORS: ABSENCE
OF THE RAGE GENE, HIGH LEVELS OF TAURINE AND
OTHER CARBONYL SCAVENGERS, AND LOW PLASMA
CONCENTRATIONS OF METHYLGLYOXAL
Authors: Szwergold B, Miller C
Presenter Institution: Deglycation Research
Normal glucose levels in blood plasma of all birds are much higher
than in humans. In addition, avian body temperatures range
between 39 oC and 42oC, they have a higher BMR, and are subjects to oxidative stresses comparable or higher than humans. In
spite of these factors, birds experience no complications comparable to diabetic humans and live longer than terrestrial animals of
comparable body sizes. For instance, pigeons with blood glucose
of ~ 20 mM have a lifespan of ~ 20 years while rats with blood
glucose of ~ 5 mM live for ~ 2 years.
In an attempt to understand avian resistance to chronic hyperglycemia, which would be very deleterious to humans, we have
elected to view birds as a pathology-free animal models of type
2 diabetes. In this presentation, we elaborate advantages of
this new perspective over traditional animal models of diabetes.
Furthermore, even in the absence of any new data, this approach
illuminates a number of biochemical differences between humans
and birds.
One of these differences is the apparent absence of an avian
homolog to the ubiquitous mammalian RAGE gene (Receptor
for Advanced Glycation End Products) that is a contributor to the
developments of diabetic complications. In our analysis of this
issue we probed completed vertebrate genomes for homologues
of the RAGE gene, using as a probe the bovine mRNA RAGE
sequence. Significant homologies were found in all the mammals
but in none of other vertebrates. This latter category included
three bird species (chicken, turkey and zebra finch).
A second difference is in the composition of blood plasma. Specifically, we noted that, compared to humans, birds have significantly
higher plasma levels of taurine and other carbonyl scavengers.
Finally, since avian erythrocytes do not use glucose as an energy
source, their glycolytic rates are about 90% lower than those of
34
humans and consequently they appear to produce significantly

lower amounts of the potent glycating agent methylglyoxal.
We therefore postulate that the remarkable avian longevity and
resistance to chronic hyperglycemia is due, in part, to these three
factors.
5. PEPTIDE-MEDIATED SIRNA DELIVERY TARGETING VEGF

EXPRESSION IN GLIOBLASTOMA AND ENDOTHELIAL CELLS
FOR ANTI-ANGIOGENIC THERAPY OF CANCER
Authors: Shubina A, Egorova A, Baranov V, Kiselev A
Presenter Institution: Department of Genetics and Biotechnology,
Saint-Petersburg State University
Cancer is one of the most common and severe age-related
diseases. The lack of efficient treatment of this disorder makes
it suitable for development of alternative gene therapeutic
approaches. One of the main features of most solid tumor cancers
is angiogenesis. Of particular importance is vascular endothelial
growth factor (VEGF), which stimulates endothelial cell migration
and proliferation. Thus, delivery of small interfering RNA (siRNA)
down-regulating VEGF expression may be a promising approach
to anti-tumor therapy. For this purpose targeted delivery system
has to be developed. To achieve targeted gene delivery, carriers
can be modified with ligand for cell-specific receptor. Previously,
we have developed peptide carriers modified with ligand to
CXCR4, a receptor overexpressed in different metastatic tumors.
We studied vehicles composed of cross-linking peptides conjugated with CXCR4 ligand and compared them to ligand-free
peptides. Physicochemical properties of the siRNA/peptide complexes were tested. We also evaluated the toxicity of siRNA/peptide complexes. Transfection efficacy of complexes was studied in
vitro on CXCR4-expressing cells, such as endothelial hybridoma
E.A.Hy926 cells and A172 glioblastoma cells. For down-regulation of VEGF expression the cells were transfected with siRNA
against VEGF. To test whether anti-VEGF siRNA delivery can
inhibit pro-angiogenic activity of endothelial cells, we evaluated
the ability of siRNA/peptide complexes to inhibit migration of
endothelial cells in vitro.
It was shown that carriers efficiently bind siRNA and protected
it from enzymatic degradation. siRNA/peptide complexes
efficiently transfected CXCR4 expressing cells and modification
of siRNA/peptide complexes with CXCR4 ligand significantly
increased their transfection efficacy. Moreover, transfection
efficacy of complexes containing peptides modified with CXCR4
ligand was significantly higher than of control complexes containing commercial transfection reagent PEI. We demonstrated
that siRNA/peptide complexes are not toxic for cell cultures.
siRNA delivery by means of ligand-conjugated carriers resulted in
2.5-3-fold decrease of VEGF expression in glioblastoma cells and
in 1.5-2-fold decrease of VEGF expression in endothelial cells in
vitro. Delivery of siRNA/peptide complexes resulted in 2-6-fold
decrease in VEGF protein production by endothelial cells. And
delivery of siRNA/peptide complexes containing CXCR4 ligand
resulted in significant inhibition of cell migration in vitro.
Poster Abstracts
The study shows that utilization of peptide carriers modified
with CXCR4 ligand is a promising approach to development of a
targeted nucleic acid delivery system to human cancer cells. Complexes containing these carriers and siRNA significantly down-regulate VEGF expression in human glioblastoma and endothelial
cells, inhibit VEGF protein production and migration of endothelial cells in vitro and thus can be used to develop anti-angiogenic
treatment for solid tumor cancers.
This work was supported by OPTEC company fellowship, RFBR
grant 12-04-31400-mol-a and by the Ministry of education and
science of Russia (no. 8142).
6. BROADLY ACCESSIBLE MICROFLUIDIC TECHNOLOGIES TO

SUPPORT MICROTISSUE ENGINEERING WITH PLURIPOTENT
STEM CELLS
Authors: Razian G, Hayden C, Ungrin M
Presenter Institution: Department of Comparative Biology and
Experimental Medicine Faculty of Veterinary Medicine University
of Calgary
Microtissue engineering the production and study of engineered tissue constructs in the sub-millimeter range is the
central focus of the Ungrin laboratory. Constructs at this scale
reveal the self-organizational capacity of cells of various types,
while avoiding the limitations on transport of oxygen and other
factors that arise when the interior of a construct is too far from
the nearest edge. In support of these goals, we are pursuing the
development of broadly accessible supporting technologies, such
as our previously released AggreWell system for the production
of large numbers of uniform three-dimensional microtissues. We
have previously published the capacity of human pluripotent
stem cells to recapitulate key aspects of early morphogenesis that
are otherwise inaccessible for study. We anticipate that an understanding of the native processes of organogenesis during human
development will be critical in order to reproduce these processes
for regenerative medicine applications. Consequently, we have
developed a widely accessible process for the generation of
microfluidic devices, usable in a conventional biological-research
laboratory. We will present the process, and discuss on-going
experiments as we begin studies of pluripotent microtissues in
this system.
7. IMPLICATIONS OF TA-65 IN CARDIOVASCULAR AND

METABOLIC HEALTH
Authors: Suram A, Singaravelu G, Patton N, Harley C, Raffaele J
Presenter Institution: T. A. Sciences
Increasing age is associated with accumulation of dysfunctional
cells. Cells with limited replicative capacity contribute to the
age-related decline in the functioning of the tissues and organs
of the body, including the cardiovascular system. Telomeres, the
ends of chromosomes, shorten every time a cell divides and
expose chromosomes to the perils of DNA damage. Very short
telomeres result in replicative senescence and dysfunctional
cells. Various research groups propose strategies to prevent
the formation of dysfunctional telomeres. Here we present an
intervention that prevents telomere dysfunction in selected

cells. Telomerase, a reverse transcriptase, is the enzyme that adds
telomere repeats to the ends of chromosomes. TA-65 is a small
molecule compound extracted from a Chinese herbal medicine,
and has been identified as a telomerase activator in an empirical screen. Extensive research was carried out in exploring the
effects of TA-65in vitro, in animal models, and in human clinical
trials. Activation of telomerase has been consistently observed in
different telomerase-competent cell types, such as keratinocytes,
lymphocytes, human colonic epithelial cells, etc. TA-65 enhances
immune function by thwarting telomere shortening, increasing
proliferative potential and anti-viral activity of cytotoxic T lymphocytes isolated from HIV infected patients. Mice studies indicate
TA-65 activates telomerase, elongates telomeres and elicits other
anti-aging effects. Telomere dysfunction causes changes in key
metabolic and cardiovascular systems. The current study reports
the effects of TA-65 on cardiovascular and metabolic profiles of
human volunteers. The potential of TA-65 as an intervention to
prevent telomere dysfunction and the metabolic derangements
caused by aging is discussed.
8. THE EFFECT OF DIETARY METHIONINE RESTRICTION ON

CARDIAC FUNCTION IN MICE
Authors: Ables G, Peffers M, Seymour H, Hampton T, Perodin F,
Augie I, Orentreich D, Orentreich N
Presenter Institution: The Orentreich Foundation for the
Advancement of Science
Dietary methionine restriction extends lifespan in rodents with
concomitant hyperhomocysteinemia, a condition that is associated with increased risk for cardiovascular disease. The paradoxical effect of homocysteine on lifespan was, therefore, assessed by
testing the cardiac function in young and old mice on the MR diet.
Young (820 weeks old, n = 78/group) and old (6074 weeks old,
n = 78/group) C57BL/6J male mice were fed a diet containing
either 0.84% methionine (control fed; CF) or 0.12% methionine
(methionine restricted; MR) for 12-14 weeks. We show that young
and old MR mice had relative cardiac enlargement and hyperhomocysteinemia compared to the CF group. In addition, plasma
levels of the sulfur amino acids: methionine, taurine and cysteine
were lower in the MR mice. Cardiac gene expression analysis
revealed upregulation of the hypertrophy markers for natriuretic
peptide A (Nppa) in young MR mice while Nppb was upregulated
in both young and old MR mice as compared to CF. Histological
analysis showed that cardiomyocyte sizes were similar in both
groups of young mice but were smaller in old MR mice than in
old CF mice. Immunohistochemistry analysis for cell proliferation
marker Ki67 was similar among all four cohorts. Non-invasive
electrocardiography (ECG) showed that, at baseline, the young
MR mice had longer QRS segments than the CF mice. However,
following an acute response to cardiac hypertrophy by -adrenergic stimulations using isoproterenol, the response was similar in
both groups of young mice. In the old mice, we found no differences between the 2 groups at baseline in all the ECG parameters.
Interestingly, while the old CF mice responded to the isoproterenol injections with longer RR, PQ, and PR segments compared
to its own baseline, the MR mice did not elicit any response
following the stimulation. To test for cardiac contractility, isolated
35
Poster Abstracts
heart retrograde perfusion tests were conducted and revealed
similar levels of response at baseline and even after calcium and
isoproterenol stimulations in both groups of old mice. Overall,
our studies suggest that MR-induced hyperhomocysteinemia
may not affect cardiac function in mice.
9. SERUM IGF-BP2 STRONGLY MODERATES AGES EFFECT

ON COGNITION
Authors: Royall D, Palmer R
Presenter Institutions: Departments of Psychiatry, Medicine,
and Family and Community Medicine; The University of Texas
Health Science Center and the South Texas Veterans Health
Administration Geriatric Research Education and Clinical Center
We have employed structural equation models of a theory driven
factor structure to produce a latent variable measure of dementia
severity. Our approach is modular, and be redirected towards the
cognitive correlates of age. It parses the observed variance in
cognitive performance into three compartments: the age-related
fraction of shared variance (dAGE), the non-AGE-related fraction
of shared variance (g, i.e., dAGEs residual in Spearmans g), and
measure specific variance (including measurement error). We
have associated dAGE with a set of serum protein biomarkers in
a well characterized cohort, the Texas Alzheimers Research and
Care Consortium (TARCC). It now becomes an empirical question
whether individual serum proteins, e.g., IGF-BP, have associations
with cognitive test performance, and if so, then whether they are
mediated via dAGE, g or independently of them. In this analysis,
we find that serum IGF-BP is strongly associated with dAGE, but
not g. Independent of its effect on dAGE, IGF-BP has moderate
positive effects on verbal measures (i.e., animal naming, verbal
fluency, and Boston Naming) and an inverse association with Trail
Making. IGF-BPs potentially beneficial direct effects on cognition
are likely to be overwhelmed by its adverse effects on dAGE. Thus,
IGF-BPs effects on cognition are complex. These findings suggest
that complete understanding of such associations may necessarily
require a latent variable approach.
10. HUMAN EVOLUTION, LIFE HISTORY THEORY, AND THE

END OF BIOLOGICAL REPRODUCTION
Author: Last C
Presenter Institution: Global Brain Institute, Vrije Universiteit
Brussel
Throughout primate history there have been three major life
history transitions towards increasingly delayed sexual maturation
and biological reproduction, as well as towards extended life
expectancy. Monkeys reproduce later and live longer than do
prosimians, apes reproduce later and live longer than do monkeys,
and humans reproduce later and live longer than do apes. These
life history transitions are connected to increased encephalization. During the last life history transition from apes to humans,
increased encephalization co-evolved with increased dependence
on cultural knowledge for energy acquisition. This led to a dramatic pressure for more energy investment in growth over current
biological reproduction. Since the industrial revolution socioeconomic development has led to even more energy being devoted
36
to growth over current biological reproduction. I propose that this

is the beginning of an ongoing fourth major primate life history
transition towards completely delayed biological reproduction
and an extension of the evolved human life expectancy. I argue
that the only fundamental difference between this primate life
history transition and previous life history transitions is that this
transition is being driven solely by cultural evolution, which may
suggest some deeper evolutionary transition away from biological evolution is already in the process of occurring.
In this paper, we are attempting to provide a multi-disciplinary
perspective on the elimination of aging (from here referred to
as radical life extension). The first thing that must be considered
when discussing radical life extension (RLE) are the practical consequences such an achievement would have on human growth
and reproduction. Popular and political opposition to RLE primarily stems from the belief that such a development would lead
to catastrophic overpopulation issues. I would like to specifically
address how human growth and reproduction should be affected
by the achievement of RLE. Such an understanding would help
us properly prepare for the resulting demographic transformation, as well as restructure popular and political dialogue around
real problems, as opposed to imagined problems. In order to
accomplish this I am proposing a straightforward methodology
dependent on A) the evolution of human growth and reproduction, B) a situation of this evolution within the explanatory
framework of Life History Theory (LHT), and C) an extrapolation
of modern developed world sexual behavior into the near-term
future (~2040-2050). With such an approach we should be able to
understand the evolved life history of humanity and how major
technological breakthroughs related to RLE should affect our
growth and reproduction patterns. Hopefully such an analysis will
give demographers, historians, anthropologists, biologists and
futurists the framework they need to better understand the future
of the human population.
11. A CASE FOR SENILITY: AGE ADVERSELY AFFECTS

COGNITION, BUT ONLY THROUGH
Authors: Royall D, Palmer R
Presenter Institutions: Departments of Psychiatry, Medicine, Family
and Community Medicine, The University of Texas Health Science
Center and the South Texas Veterans Health Administration
Geriatric Research Education and Clinical Center
We have employed structural equation models (SEM) to explicitly
distinguish functional status, and therefore dementia-relevant
variance in cognitive task performance (i.e., for dementia).
Regardless of the sample frame and /or the measures used
to construct it, appears to be strongly related to dementia
severity, and accurately distinguishes dementia from both Mild
Cognitive Impairment (MCI) and controls. In this study, we test
ages association with in a Multiple Indicators Multiple Causes
(MIMIC) model. Ages adverse effects on cognition are entirely
mediated through , independent of education, ethnicity, gender,
depression ratings, serum homo-cysteine levels, hemoglobin
A1c, and apolipoprotein e4 status. This suggests that normative
aging is a potentially dementing condition (i.e., a senility). It also
constrains ages adverse effect on cognition to the age-related
Poster Abstracts
fraction of general intelligence (Spearmans g). That finding
has biological and pathophysiological implications. Future studies
can now identify the biomarkers that mediate the association
between age and scores. Those might offer opportunities for
the specific remediation, modulation or prevention of age-related
cognitive disability.
12. THE USE OF STEM CELLS FOR A HEALTHIER START TO

LIFE FOR THE DISABLED CHILD
Author: Verma V
Presenter Institution: International Centre for Advocacy Auckland
Man has been trying to understand, philosophize, and address
disability in various ways through the use of prayer, technology,
and now biotechnology. Stem cells appear to have a great potential for serving children with disability. This poster will cover recent
advances in the experiments on understanding the use of stem
cells in animal models to enhance the quality of life of disabled
children. Stem cells have the potential to reverse hypoxemic-ischemic injury to the brain through stimulating recovery of neural
tissue in the brain. We are in the exciting stage of trying to get a
better understanding of these mechanisms. This poster will also
address further areas of research being done to use this significant
tool of stem cell therapy, to give disabled children in the world a
healthier start to life. This poster will also address the legal and
ethical issues in the use of stem cells for children with disability.
13. AGE-RELATED ALTERATIONS IN HUMAN

HEMATOPOIETIC STEM AND PROGENITOR CELLS
Authors: Rundberg Nilsson A, Bryder D, Pronk C
Presenter Institution: Lund University, Institution for Experimental
Medical Research
Aging of the human hematopoietic system is often associated
with decreased bone marrow cellularity, reduced adaptive
immune responses, increased incidence of anemia and an increasing risk for myeloid diseases. Similar observations were made in
mice and have been shown, at least in part, to originate already
at the hematopoietic stem cell (HSC) level. Current knowledge
on age-related alterations of the hematopoietic system is to a
large extent based on studies of the murine system. Studies on
the consequences of aging in the human hematopoietic system
remain limited and have to some extent been contradictory. We
therefor decided to further detail human hematopoietic aging
and compared adult bone marrow samples from young and old
individuals as well as cord blood cells for a number of parameters.
We observed similar changes as reported in the murine system,
including a functional decline in the proliferative and cloning
potential of HSCs, as well as impaired lymphoid cell production
with age. Furthermore, using flow cytometry, we revealed that
HSCs were increased in frequency during aging as well as in
adult bone marrow compared to cord blood. This likely reflects a
decreased output/potential from single HSCs with age. Common
lymphoid progenitors (CLPs) showed a reverse pattern from
HSCs, decreasing with age and from cord blood to bone marrow.
Adult bone marrow granulocyte/macrophage progenitors (GMPs)
decreased with age, however the frequencies in adult bone
marrow were higher compared to cord blood. Megakaryocyte/

erythrocyte progenitors (MEPs) were lower in young adult bone
marrow compared to cord blood and increased with age in adult
bone marrow. Additionally, transcriptome profiling of aged HSCs
demonstrated a skewing towards GMP/MEP-associated genes,
while lymphoid-associated genes were downregulated. This
indicated that, similar to mice, the phenotypes associated with
human hematopoietic aging could be linked to changes in the
very primitive HSC compartment.
14. EPIGENETICS: PROMISING RESEARCH IN THE

PROGRESSION AND TREATMENT OF ALZHEIMERS DISEASE
Author: Mukti R
Presenter Institution: Mawlana Bhashani Science and Technology
University
Epigenetics holds great promise to resolve and explain many
unsolved questions and issues in modern biology. Epigenetics is
the reversible inherited changes in gene expression that occurs
without any alteration in DNA sequence. As epigenetic modifications can be reversed by nutrients or drugs or other environmental factors, the design of more rational interventions to target
or detect epigenetic changes is expected in the near future to
complement the science of genomics in making new inroads to
effective personalized medicine. Alzheimer disease (AD) is the
most common form of dementia that causes memory loss and
problems with behavior and other intellectual abilities, serious
enough to interfere with daily life. AD is caused by hypomethylation and increased histone acetylation of APP (amyloid precursor
protein) promoter. Aberrant miRNA-mediated processing of
mRNA can lead to abnormal levels of mRNA and consequent
neuronal dysfunction in AD brain hippocampus. Environmental
cues such as diet, metal exposure, maternal care and intrauterine
exposures may perturb gene regulation during early development
causing epigenetic dysregulation and contribute to the pathogenesis of AD. The knowledge about the role of epigenetics in
the progression of this neurodevelopmental disorder provides a
perfect opportunity to design rationale therapeutic strategies, for
example, contextual memory deficits can be completely reversed
by the administration of histone deacetylases.Epigenetics holds
great promise to resolve and explain many unsolved questions
and issues in modern biology. Epigenetics is the reversible
inherited changes in gene expression that occurs without any
alteration in DNA sequence. As epigenetic modifications can be
reversed by nutrients or drugs or other environmental factors, the
design of more rational interventions to target or detect epigenetic changes is expected in the near future to complement the
science of genomics in making new inroads to effective personalized medicine. Alzheimers disease (AD) is the most common form
of dementia that causes memory loss and problems with behavior
and other intellectual abilities, serious enough to interfere with
daily life. AD is caused by hypomethylation and increased histone
acetylation of APP (amyloid precursor protein) promoter. Aberrant
miRNA-mediated processing of mRNA can lead to abnormal
levels of mRNA and consequent neuronal dysfunction in AD
brain hippocampus. Environmental cues such as diet, metal
exposure, maternal care and intrauterine exposures may perturb
gene regulation during early development causing epigenetic
37
Poster Abstracts
dysregulation and contribute to the pathogenesis of AD. The
knowledge about the role of epigenetics in the progression of this
neurodevelopmental disorder provides a perfect opportunity to
design rationale therapeutic strategies, for example, contextual
memory deficits can be completely reversed by the administration of histone deacetylases.
15. THE HIGH OXIDATIVE STRESS RESISTANCE OF RPE CELLS

DIMINISHES LIPOFUSCIN ACCUMULATION
Author: Karlsson M, Kurz T
Presenter Institution: Division of Drug Research, Department of
Medical and Health Sciences, Linkping University
Postmitotic retinal pigment epithelial (RPE) cells phagocytose
on a daily basis the expended tips of the photoreceptors in the
eye. Residing in the retina, RPE cells live in an oxygen-enriched
environment and degrade substantial amounts of lipid-rich material. All these are prerequisites for the formation of lipofuscin, the
non-degradable age pigment whose accumulation in RPE cells
is a risk factor for development of age-related macular degeneration (AMD) - the eye disease that causes most cases of central
visual impairment in the western world. Interestingly, RPE cells
accumulate lipofuscin only late in life. We have previously shown
that cells of the immortalized RPE cell line ARPE-19 are remarkably
resistant against oxidative stress compared to another professional scavenger cell line J774. We investigated possible causes
for the oxidative stress resistance of ARPE-19 cells in comparison
to the moderately sensitive J774 cells and found: (1) similar H2O2
degradation efficiency and total as well as lysosomal iron in both
cell types, (2) tight iron binding that yet allows for survival/proliferation even under conditions of iron starvation of RPE cells, (3)
much enhanced basal levels of the iron-binding proteins metallothionein, HSP70 and ferritin as well as a high capacity for upregulation of metallothionein and ferritin in RPE cells. A constant
autophagic influx of these three iron-binding proteins into the
lysosomal compartment would keep the redox-active iron level
invariably low and prevent intralysosomal formation of hydroxyl
radicals, explaining why RPE cells tolerate high doses of oxidative
stress and accumulate lipofuscin only late in life.
16. SYSTEMS BIOLOGY OF HUMAN AGING: NETWORK

MODEL PRIMARY TABS
Author: Furber J
Presenter Institution: Legendary Pharmaceuticals
This network diagram is presented to aid in conceptualizing
the many processes of aging, the causal chains of events, and
the interactions among them. Contemplation of this network
suggests promising intervention points for therapy development. This diagram is maintained on the Web as a reference for
researchers and students. Content is updated as new information comes to light.
At first glance the network looks like a complicated web. However, as a conceptual summary, in one view, we can see how
most biogerontological processes relate to each other. Importantly, examination of these relationships allows us to pick out
38
reasonably plausible causal chains of events. Within these chains,

we can see age-related changes or accumulations that appear to
be promising targets for future therapy development. The many
observable signs of human senescence have been hypothesized
by various researchers to result from several primary causes.
Inspection of the biochemical and physiological pathways associated with age-related changes and with the hypothesized causes
reveals several parallel cascades of events that involve several
important interactions and feedback loops. This network model
includes both intracellular and extracellular processes. It ranges in
scale from the molecular to the whole-body level. Effects due to
externalities, lifestyle, environment, and proposed interventions
are highlighted around the margins of the network.
17. AGING IS INEVITABLE BUT IS IT AVOIDABLE?

Authors: Augsburger B, Irwin M
Presenter Institution: Department of Pathobiology, College of
Veterinary Medicine, Auburn University
Every biomolecule is subject to the second law of thermodynamics, which applies constant pressure towards degeneration.
The low entropy state in living organisms is maintained only
through the combination of: 1) activation energy requirements
for breaking chemical bonds, and 2) the directed investment of
additional energy to repair and replace biomolecules. A prospective approach was applied towards characterizing the inevitability
of biomolecular degradation in mammalian organisms. Such
degradation is ubiquitous in aging, yet a causal diagram of the
aging process and the relative positioning of the various classes
of damaged biomolecules in this diagram have yet to be firmly
established.
A thermodynamic analysis of mammalian genetic molecular
fidelity was performed, with consideration given to known biomechanisms and utilization of transition state theory. The temporal
and spatial distribution of the genetic molecules in an organism
throughout a full lifespan was also considered in the analysis.
Thermodynamic system boundaries were modelled based on
mammalian organismal biology. Germline genetic molecular
integrity was similarly analyzed.
The results demonstrate that the nuclear and mitochondrial
genetic molecular fidelity of a mammalian organism are destined
to be compromised with time. In other words, the degradation of
nuclear and mitochondrial DNA is certain, given sufficient time. An
additional analysis demonstrates how germ cells, through somewhat different mechanisms, are able to maintain nuclear DNA
integrity and effectively reset mitochondrial DNA populations to
healthy, homogeneous states typical of a youthful organism.
The degradation of other classes of biomolecules is also
considered. Similar analyses demonstrate how pools of these
molecules can, in theory, be maintained with perfect fidelity,
provided genetic fidelity is maintained; thus, they are not by
necessity top level contributors to aging. Also discussed are
hypothetical biomechanisms that, if present in an organisms
genome, could potentially overcome the inevitability of genetic
molecular degradation.
Poster Abstracts
Although genetic molecular fidelity reduction is inevitable
given the current evolutionary state of mammals, the amount of
energetic resources an organism invests into maintaining genetic
fidelity can modulate the rate of decay but with diminishing
returns. Considering that cellular energy spent on genetic fidelity
is unavailable for other processes, species have evolved in a way
that balances the requirement for maintaining genetic fidelity
with other energy consuming processes, thus establishing a
compromise between lifespan and other factors that provide
selective advantage.
The results of these analyses provide important insight into the
causal relationships of different classes of biomolecular degradation in the aging process. Establishing a hierarchal causal diagram
of the aging process is important for a number of reasons. The
multitude of aging theories, the discontinuities between them,
and the failure of the scientific community to agree on root causes
of aging has hindered public acceptance of the feasibility of aging
research as a means to extend useful lifespan. This discourages
investment. Beyond contributing towards public acceptance, a
clearer understanding of the causal relationships involved in the
aging process, by definition, helps distinguish between cause
and effect, and thus is valuable in the identification of potential
targets for therapies.
18. A SHORT REVIEW OF POSSIBLE USE OF CURCUMA

LONGA LINN., PIPER LONGUM LINN., AND GHEE IN THE
PREVENTION OF ALZHEIMERS DISEASE
Authors: Joseph M, Mohan P
Presenter Institution: AVP Research Foundation
The objective of the study is to compile the evidence from the
literature indicating possible use of Curcuma longa Linn., Piper
longum Linn., and ghee as a combination in the prevention of
Alzheimers disease.
The properties of C. Longa Linn., P. longum Linn., and ghee were
assessed by careful study of classical literature and research
papers searched from the PubMed database, EBSCO Host and
Science Direct databases and Google Scholar for studies that
provide evidence for their use in the prevention of Alzheimers
disease. These substances were found to be ingredients in various
combinations in quite a number of Recipes lending support to
the efficacy of the combination in Alzheimers disease. This effect
was made explainable by modern principles like the action of
curcumin (chemical constituent of Curcuma longa Linn.) on the
Alzheimers disease, the action of piperine (chemical constituent
of Piper longum Linn.) in increasing bioavailability of curcumin
and the action of lipid in crossing the blood brain barrier to target
the drug on neurons.
The ghee processed with C.longa Linn. and P.longum Linn. seems
to have a potential for prevention of Alzheimers disease based
on this short review. This preparation should be evaluated for
its efficacy in preventing the progression of Alzheimers disease
diagnosed in the early stages.
The ghee processed with C.longa Linn. and P.longum Linn.

appears to be a potential prevention for Alzheimers disease. The
literature study on this ghee preparation and its effects on Alzheimers disease shows scope to do a preclinical and clinical study to
establish its effect on Alzheimers disease.
19. SIRT7 REGULATES A STRESS RESPONSE IN

HEMATOPOIETIC STEM CELLS
Authors: Mohrin M, Liu Y, Shin J, Brown K, Luo H, Haynes C, Chen D
Presenter Institution: University of California, Berkeley
SIRT7, one of seven mammalian homologs to the longevity gene
SIR2, negatively regulates gene expression by deacetylating lysine
18 of histone H3 (H3K18Ac), and modulates expression of genes
involved in protein biosynthesis, such as ribosomal proteins and
translation factors. SIRT7 localizes to the nucleus and is highly
expressed in the liver and hematopoietic system. All the cells of
the hematopoietic system are derived from hematopoietic stem
cells (HSCs). With advanced age hematopoietic malignancies
increase and hematopoietic function declines. SIRT7 expression
is decreased in old HSCs. Furthermore, SIRT7 is also known to
localize to a chromosomal region deleted in leukemia, and loss
of function of ribosomal proteins many of which are targets of
SIRT7 is associated with hematopoietic malignancies. To understand the role of SIRT7 in the hematopoietic system we set out to
characterize SIRT7 deficient mice. We found that SIRT7 deficiency
causes reduced quiescence, increased mitochondrial mass, and
compromised regenerative capacity of HSCs. We confirmed that
expression of SIRT7 is reduced in aged HSCs and discovered that
SIRT7 upregulation improves the regenerative capacity of aged
HSCs. Together, these data suggest that SIRT7 is part of a stress
response system that regulates HSC maintenance, and establishes
the deregulation of this SIRT7 pathway as a contributing factor
for HSC aging. Our future directions are to uncover the stress
response genes targeted by SIRT7 that regulate mitochondrial
biogenesis and metabolic function in HSCs.
20. ELUCIDATING THE ROLE OF TGF- SIGNALING IN

HUNTINGTONS DISEASE
Author: Karen R
Presenter Institution: Buck Institute for Research on Aging
Huntingtons disease (HD) results from an expansion in the number of CAG repeats in the first exon of the huntingtin (HTT) gene. It
is characterized by impairments of motor function, psychological
disturbances, personality changes, chorea, and cognitive decline.
HD patients display a loss of neurons in the striatum and cortex
associated with the toxicity of mutant HTT (mHTT) protein. There
is no cure or effective treatment to alter HD progression and
mechanisms of the disease are not completely understood. Our
lab has generated a human stem cell model of HD using human
induced pluripotent stem cells (iPSCs) to generate human neural
cells in vitro. Using homologous recombination, we corrected
HD patient-derived iPSCs to generate isogenic, corrected iPSCs
with normal CAG repeat length. Using these isogenic stem
cells, we identified phenotypes specific to mHTT including
elevated caspase activity, reduced BDNF protein, mitochondrial
39
Poster Abstracts
dysfunction, and altered signaling pathways, including cadherin
and transforming growth factor-beta (TGF-), in HD neural stem
cells (NSCs). The TGF- signaling pathway has been implicated in
various neurodegenerative diseases but thus has been minimally
studied in HD. Our goal is to identify the role that altered TGF-
signaling plays in the pathogenesis of HD. Thus far we have identified differences in levels of TGF- signaling molecules using RNAseq and qPCR analyses of HD and corrected NSCs derived from our
isogenic iPSCs. Furthermore, we find that TGF-1 is neuroprotective in HD NSCs and reduces levels of caspase-3/7 activity. Lastly
we show that the latent TGF- complex is processed differently in
mutant HD and wild type 293 cells indicating a potential mechanism for altered TGF- expression in HD cells. By elucidating the
role of TGF- signaling in HD stem cell models, we will provide a
further understanding of mechanisms leading to HD and hope to
identify new therapeutic targets to benefit HD patients.
21. ENHANCED PRIMARY ENDOTHELIAL CELL ATTACHMENT

VIA ANTIBODY CONJUGATION: TOWARD KIDNEY
IMPLANTATION USING AUTOLOGOUS CELL SOURCES
Authors: Bassin E, Huling J, Ko I, Yoo J, Atala A
Presenter Institution: Wake Forest Institute for Regenerative
Medicine
The only definitive treatment for end stage renal disease is
renal transplantation. However, a shortage of kidney donors
has created long waiting lists for patients. Recent progress in
whole organ engineering techniques based on decellularization/
recellularization suggests that this method could eventually be
used in transplantation. Although the previous approaches have
made important progress that enabled small organ constructs to
be implanted in vivo, these approaches are limited to short-term
assessments. One major challenge for long-term in vivo success
of bioengineered organs is vascular patency. In the absence of
complete endothelial reseeding of vascular matrices, significant
thrombosis is likely to occur within the vasculatures of the scaffold.
To address this issue, the WFIRM team previously developed
an endothelial cell seeding method, combined with antibody
conjugation that permits effective coating of the vascular matrix
of decellularized porcine kidney scaffolds. The WFIRM team
demonstrated the effectiveness of antibody-conjugation-mediated re-endothelialization using a xenogeneic endothelial
cell line through an in vitro cell detachment test and an in vivo
implantation test. Toward clinical translation, we aim to test the
feasibility of kidney implantation using autologous cell sources of
a functionally re-endothelialized and human-scaled porcine renal
scaffold. It is hypothesized that conjugating CD31 antibody to the
decellularized vascular matrix will improve primary endothelial
cell (pEC) attachment following implantation. To test this hypothesis, we performed a cell detachment test using a flow chamber
system to determine effects of CD31 antibody conjugation on the
improvement of pEC attachment.
As cell sources, porcine pEC were used after isolation and expansion. To characterize endothelial cell phenotypes, the expanded
cells were immunostained for CD31 and VE-cad. To prepare
antibody conjugated glass surfaces, CD31 antibody was conjugated onto collagen-coated glass slides using EDC/NHS chemistry.
40
To assess cell detachment, a flow chamber system was designed

using a commercially available device. The glass slides were
placed in the chamber and protein blocked using BSA solution.
pEC at a concentration of 7.5 105 cells/ml was introduced to the
slides and allowed to attach. The pre-adhered cells were exposed
to various physiological flow conditions and the flow experiment
was video-recorded. The number of cells on the glass slides were
counted using Image J.
Immunostaining results demonstrate that the expanded endothelial cells expressed CD31 and VE-cad positive on their surfaces. To
examine the effects of antibody conjugation on improvement of
pEC attachment, the level of cell detachment from the surfaces
under flow conditions was determined. At the lowest flow rate of
18 ml/hr, 97% of cells remained attached on antibody conjugated
slides, while 43% of cells remained on the untreated surface. With
increasing of flow rate, more than 90% of the original pre-attached cells detached from the untreated surfaces. However, the
cells on the antibody conjugated surfaces remained above 70% of
cell attachment (Two-way ANOVA, p<0.001). These results suggest
that CD31 antibody conjugation may improve primary endothelial
cell attachment under physiological flow conditions.
22. MITOCHONDRIAL DYSFUNCTION-ASSOCIATED

SENESCENCE RESULTS IN A NON-CANONICAL SECRETORY
PHENOTYPE
Authors: Wiley C, Velarde M, Freund A, Sarnoski E, Shirakawa K,
Verdin E, Campisi J
Loss of mitochondrial function is a potential vector for age-related
tissue decline. Despite ample evidence linking mitochondrial
dysfunction to age-related phenotypes in nerve and muscle, less
is known of the mechanisms behind this link in mitotically active
tissues. One potential mechanism for the age-related decline of
proliferating tissues is cellular senescence. Cellular senescence
results in permanent mitotic arrest, but may also result in the
secretion of a myriad of biologically active factors collectively
known as the senescence-associate secretory phenotype, or SASP.
We identified mitochondrial dysfunction as an inducer of cellular
senescence. Multiple mitochondrial manipulations - including
targeted knockdowns of mitochondrial proteins, depletion of
mitochondrial DNA, and inhibition of the electron transport chain
- resulted in senescence, but that senescence response lacked
canonical secretory phenotypes, especially the IL-1 inflammatory
arm of the SASP. Cells induced to senescence in this manner
displayed altered NAD+/NADH ratios, and both senescence arrest
and secretory phenotypes could be rescued by manipulations
that restored NAD redox balance. Altered NAD redox balance
resulted in P53 phosphorylation in an AMPK-dependent manner,
and activation of P53 was required for both senescence and
suppression of the IL-1 inflammatory arm of the SASP. Senescent
cells also accumulated in the adipose tissue of progeroid mice that
rapidly accrue mitochondrial DNA mutations (POLGD257A mice),
and the secretory profile of those tissues closely resembled that of
human fibroblasts during mitochondrial dysfunction, indicating
that these phenotypes can also occur in vivo. These data provide a
Poster Abstracts
novel link between mitochondrial dysfunction and aging through
the process of cellular senescence.
23. EXPOSURE TO AN ENVIRONMENTAL TOXIN ASSOCIATED

WITH PARKINSONS DISEASE INDUCES ASTROCYTIC
SENESCENCE WITHIN THE SUBSTANTIA NIGRA AND LEADS
TO DOPAMINERGIC CELL LOSS
Authors: *Woods G, *Chinta S, Rane A, Zou Y, Demaria M, Campisi J,
Andersen J
Parkinsons disease (PD) is a neurodegenerative disease characterized by the loss of dopaminergic (DAergic) neurons within a
region of the midbrain known as the substantia nigra (SN). PD is
thought to arise from the combined effect of susceptible genetic
backgrounds and repeated exposure to environmental insults.
In particular, exposure to the herbicide, paraquat (PQ), has been
linked to the development of PD. Yet, the single largest risk factor
for acquiring PD is advanced age. As tissues age and cancer risks
amass, mitotic cells can undergo cellular senescence, a tumor
suppressive mechanism which induces near permanent mitotic
arrest. However, the accumulation of senescent cells on its own
is thought to directly contribute to the physiology of aging and
its associated diseases. Evidence suggests that glial cells undergo
senescence over time in the brain and that this may contribute to
age-related neuropathologies. Therefore, we tested the possibility
that PQ administration induces glial senescence, hypothesizing
that the accumulation of senescent glia could itself contribute to
eventual DAergic cell loss.
We found that exposure of mice to PQ caused neurodegeneration
of DAergic cells in the SN, which was accompanied by hallmarks of
cellular senescence in the SN proper. PQ administration caused SN
resident astrocytes to undergo cellular senescence as evidenced
by a loss of laminB1 and HMGB1 expression in GFAP positive
cells. Ablation of senescent cells, using a mouse model in which
senescent cells can be inducibly eliminated in vivo, was protective
against PQ induced Parkinsonian pathologies. Thus the accumulation of senescent astrocytes, as a result of aging or exposure to
toxins, may mechanistically contribute to the development of PD.
Support: T32 (GW), Ellison Senior Scholar Award (JKA), Marin
Community Foundation (JKA/JC)
* co-first authors
24. NEUROPEPTIDE SIGNALING AND HEALTHSPAN INC.

ELEGANS
Authors: Aguiar S, Liang T, Adams N, Tseng J, Garrison J
Presenter Institution: The Buck Institute for Research on Aging
Genetic manipulation has enabled the five-fold extension of C.
elegans lifespan (Chen et al., 2013). This synergistic elongation
was accomplished by mutating only two genes: rsks-1 (TOR) and
daf-2 (insulin receptor). The search for additional life-extending
genes is ongoing.
Neuropeptides (NPs) are modulatory intercellular signaling

molecules secreted exclusively by neurons, and may coordinate
organismal aging. NPs, such as brain-derived neurotropic factor
(BDNF) and gonadotropin-releasing hormone (GnRH), have been
shown to play a role in cell survival and systemic inflammaging,
respectively. However, the role of other NPs in aging is a relatively
new area of inquiry.
The hypothalamus secretes a number of neuropeptides putatively
relevant to aging, including vasopressin (AVP), and oxytocin (OXY).
The former has been shown to regulate water retention and the
latter social cognition and the rate of muscle regeneration in mice
(Elabd et al., 2014).Recently, the nematodeC. eleganswas found to
possess an AVP/OXY ortholog, known as nematocin (Garrison et al.,
2012). Research on this NP is just beginning. It is known that male
worms require nematocin to mate properly, but it is unknown
whether this newly discovered NP plays any role in aging.
This project will evaluate the effect of nematocin knockout on
mean lifespan (comparing automated and manual assays), muscle
tissue degeneration (sarcopenia), and thermotolerance. The
primary aim of this study is to determine whether nematocin is
involved in longevity.Secondarily, sarcopenia testing bears upon
whether the putative muscle-rejuvenating activity of oxytocin is
conserved in C. elegans. Third, thermotolerance data may provide insight as to whether neuropeptide KOs are living longer or
shorter lives due to altered stress resistance versus a genetically
programmed longevity clock that operates irrespective of stress.
25. EVALUATION OF ENGRAFTMENT OF HUMAN MSC

ENGINEERED TO ENHANCE IMMUNOMODULATORY
POTENTIAL IN A MURINE MODEL OF INFLAMMATORY
BOWEL DISEASE, THROUGH CONFOCAL MICROSCOPY
Authors: Crowley C, Mokhtari S, Vance M, Rodman C, Marrs G,
Porada C, Almeida-Porada G
Medicine
Inflammatory Bowel Disease, (IBD), is a group of disorders
characterized by inflammation of the gastro-intestinal tract due to
an altered immune response. Despite affecting nearly 1.5 million
individuals in the U.S. and 2.2 million individuals in Europe, no
treatment option thus far has emerged as a successful cure to this
disease. Today, many cellular based therapies are being considered as a potential treatment for IBD. Of particular interest, mesenchymal stromal cells (MSCs) have been shown to migrate, upon
infusion, to areas of inflammation, where they release soluble
factors to promote healing, inhibit apoptosis, and stimulate/support resident stem/progenitor cells. Yet, only 30% of IBD patients
in clinical trials respond to MSC therapy.
Here, we hypothesized that transplantation of MSCs engineered
to enhance their inherent immunomodulatory potential and/or
to increase homing would improve the ability of MSCs to
migrate to the intestine and enhance their therapeutic potential.
Therefore, we used a T cell transfer model in Balb/c-scid mice to
replicate IBD-like disease and treated the animals with one of
three different human MSC (hMSC) cell lines: unmodified hMSC,
41
Poster Abstracts
hMSC modified to increase their anti-inflammatory potential
through HLA-G1, or hMSC modified with improved anti-inflammatory potential and improved migratory specificity to the intestinal
crypts through HLA-G1 and Eph-B2.
Large intestine samples (Cecum) from transplanted animals (n=12)
were harvested approximately 3 month after therapy. Negative
control animals consisted of age-matched mice in which no disease induction or cell therapy was performed (n=3). Tissues were
paraffin embedded after which they were cut, mounted on slides,
and stained to image via confocal microscopy. The staining was
performed using a mouse on mouse (M.O.M.) kit and antibody
specific to human mitochondria. Samples were counterstained
with DAPI to visualize nuclei within the cells. A LSM Zeiss 710
confocal microscope was used with 10x and 40x oil magnifications
to visualize the tissue samples from each of the 15 animals. High
levels of human MSC engraftment were seen in animals transplanted with all MSC populations. However, the highest levels of
engraftment were observed in mice treated with hMSCs modified
with HLA-G1, whereas animals transplanted with Eph-B2 showed
the lowest levels of engraftment.
Because transfer of mitochondria can occur as part of the regenerative process mediated by MSC, future studies will determine
whether cells displaying human mitochondrial staining are indeed
human MSC that engrafted in the intestine or are murine cells
containing transferred human mitochondria. Therefore, fluorescent in situ hybridization (FISH) using probes specific for human
DNA will be performed simultaneously with human mitochondria
detection in a protocol that we are currently optimizing. Furthermore, we will continue to stain for immune cell activity using
CD8 and CD25 antibodies, which will give us a better look at the
altered immune state within the IBD mouse, specifically those
treated with our different cell lines.
26. EVALUATION OF ENGRAFTMENT AND APOPTOSIS

FOLLOWING TRANSPLANTATION OF MODIFIED HUMAN
BONE MARROW MESENCHYMAL STROMAL CELLS IN A
MURINE MODEL OF INFLAMMATORY BOWEL DISEASE
Authors: Hawkins A, Soland M, Rodman C, Porada C, AlmeidaPorada G
Medicine
Inflammatory Bowel Disease (IBD) comprises a group of chronic
inflammatory conditions of the gastro-intestinal tract, the most
common forms of which are Crohns disease and ulcerative colitis.
IBD is a significant and rapidly growing health care burden that
affects more than 1.5 million people in the US alone. Although
several therapies to induce remission and/or to prevent relapse
exist, the side effects, toxicity, and lack of response many patients
experience highlight the urgent need to develop a cure for this
devastating and costly disease.
Our goal is to develop novel cell-based therapies that could
promise a curative treatment for IBD. We have based these
therapies on mesenchymal stromal cells (MSC) due to the innate
ability of MSC to home to areas of inflammation and produce both
42
immunomodulatory factors and trophic factors that stimulate

endogenous repair/regeneration within injured/diseased tissues.
Unfortunately, many of the infused MSC never make it to their
desired target tissue following administration. Moreover, despite
their anti-inflammatory properties, those that do arrive to the
site of injury are often unable to completely reset the abnormal
immune response. To overcome these barriers, we modified
human MSC to overexpress immunomodulatory factors and molecules that increase their ability to home to the large intestine. To
begin testing the therapeutic potential of these cellular therapies,
we generated an adoptive T cell transfer-induced murine model
of IBD that accurately recapitulates many of the inflammatory and
immunological aspects of human IBD.
We then used this model to evaluate the therapeutic potential of
three populations ofhuman bone marrow MSC: 1) unmodified
MSC 2) MSC overexpressing immunomodulatory factors; and
3) MSC overexpressing both immunomodulatory factors and
homing molecules. Following injections of the various MSC
populations, we noted a marked clinical improvement in many
of the animals receiving the modified MSC. Following euthanasia,
we examined the intestinal tissue from the animals to determine
whether a correlation exists between the degree of clinical
improvement and the levels of MSC engraftment within the
intestine and to ascertain whether MSC engraftment resulted in a
reduction in the levels of apoptosis occurring within the intestinal
mucosa and/or an increase in apoptosis in the resident autoreactive T cells. To determine the extent of engraftment within
the large intestine, we performed quantitative PCR (qPCR) with
primers specific to human GAPDH. While all 3 cell populations
successfully engrafted the IBD intestine, the levels of engraftment differed among the 3 groups. To evaluate the effect of the
engrafted cells on the incidence of apoptosis, we performed Western blotting for Caspase-3, an enzyme that is activated in apoptotic cells, on protein extracts from the large intestine. Mice that
received MSC overexpressing both immunomodulatory factors
and homing molecules exhibited the highest levels of Caspase-3,
while mice that received MSC overexpressing immunomodulatory
factors had the lowest levels. Further studies employing immunohistochemistry will determine whether the apoptosis is occurring
in epithelial cells or resident autoreactive T cells. We are also performing cytokine arrays to understand how our cell therapy has
affected the aberrant cytokine production that characterizes IBD.
27. SENESCENCE, CANCER, AND HYPOXIA-INDUCIBLE

FACTOR
Authors: Harper M1, Demaria M1, Campisi J1,2
Presenter Institutions:
Buck Institute for Research on Aging
2
Lawrence Berkeley National Laboratory
Aging promotes both degenerative pathologies, characterized by

loss of tissue or cellular homeostasis, and hyperplastic pathologies,
such as cancer, in which cells develop new, detrimental functions.
These seemingly contrasting pathologies may both be affected
by an antagonistically pleiotropic response to genotoxic stress,
termed cellular senescence. Though senescence has been linked
to both cancer and aging, the mechanisms by which senescence is
Poster Abstracts
regulated and the effect of senescence on these diseases has yet
to be fully determined. Cellular senescence is a state of irreversible
growth arrest that serves as a tumor-suppressive mechanism.
Senescent cells experience deep morphological and functional
changes, and they activate a transcriptionally-regulated secretory
program known as the senescence-associated secretory phenotype (SASP). The SASP includes several proinflammatory factors
with strong paracrine activity for which levels are elevated during
aging and cancer treatment.
The hypoxia-inducible factor (HIF)-1a is one of the transcription
factors that participate in the senescence program. Under normal
conditions, HIF-1a responds to oxygen levels to promote the
formation of new blood vessels in hypoxic conditions. Here, we
compared HIF-1a knockdown and control cells for induction
of senescence and levels of SASP factors. Levels of HIF-1a were
compared at hypoxic (1%), normoxic (3%), and atmospheric (20%)
oxygen concentrations. HIF-1a is expected to be present in tissue
traditionally low on oxygen, such as tumor masses. This experiment examined whether oxygen levels similarly played a role in
induction of senescence and control of the SASP. All together, the
data indicates the connection between HIF-1a, senescence, and
oxygen concentration.
Together with aging, standard anticancer treatments, such as
chemotherapy and irradiation, induce senescence in the tissue
microenvironment. These therapeutic approaches may cause a
senescence-dependent cancer recurrence or accelerated aging
through the disruption of normal tissue functions. Here, we look
at varying chemotherapy drug concentration for induction of
senescence, and we define the importance of counteracting the
senescence phenotype upon anti-cancer treatments to limit
adverse effects of the therapies.
28. RESPONSE OF ROBO1-DEFICIENT HUMAN RPE CELLS TO

PHYSICAL DAMAGE
Authors: Liker K, Goldin E
Presenter Institution: SRF Research Center
Age-related macular degeneration (AMD) is the leading cause
of adult blindness in developed countries, yet scientists know
relatively little about how AMD begins and progresses to visual
impairment. Available treatments for the disease target mainly
one type of AMD (neovascular or wet AMD) and do not successfully treat early stage AMD or the dry form known as geographic
atrophy. Studies often use rodent models to study AMD, but
model organisms are not always ideal systems for developing
human treatments. Additionally, human trials can be costly and
dangerous. We propose a cell model of AMD using mature human
retinal pigment epithelial (RPE) cells to study genes implicated in
AMD and potential AMD treatments. This model will give us a safe,
cost-effective, and realistic model for better characterizing the
behavior of diseased RPE cells and the effects of genes involved in
the RPE extracellular matrix (ECM) and lipid transport.
RPE cells supply photoreceptor cells with nutrients, process the
photoreceptors light-transducing outer segments that are shed
daily, and are involved in recycling retinoids, which are essential
chemical components for vision processing. Experts believe that

in AMD, dysfunction or death of RPE cells contributes to the death
of photoreceptors, vision loss, and the formation of drusen, which
are lipid deposits characteristic of AMD. However, RPE cell cultures
that mimic AMD have rarely been created since there is disagreement in the scientific community regarding whether aged RPE
cells accurately represent AMD.
Our RPE cells will mimic AMD through RNAi knockdown of three
genes associated with both human and rodent versions of AMD.
Two of these genes code for transmembrane proteins significant
in lipid and nutrient transport. In AMD, reduced lipid and nutrient
transport could contribute to the buildup of the lipid deposits
inside drusen and the viability of RPE cells. The final gene of
interest is ROBO1, an extracellular matrix (ECM) protein in RPE
cells. Cells deficient in ROBO1 are known to be less adherent, to
migrate poorly, and to proliferate poorly. The inability of RPE cells
to migrate could be a cause of AMD: loss of motion could prevent
the replacement of old RPE cells by new RPE cells that migrate
from the periphery of the macula. The macula is the central part
of the retina and is responsible for acute vision. If new cells are
unable to replace old RPE cells, then the macula may degenerate
as seen in AMD. We will perform a physical damage assay to test if
ROBO1 is necessary for RPE cell migration and proliferation. If the
cells with impaired ROBO1 function show reduced cell proliferation and healing compared to healthy RPE cells after damage,
then ROBO1 could be a new target for AMD therapies.
Once all of the RNAi cell lines are established, the team plans to
use these cells to test the response of cells to lysosomal treatments. Researchers propose that lysosomal dysfunction could be
a contributing factor to drusen-related lipid buildup. By restoring
lysosomal function to our model, the team hopes to reduce this
intracellular waste accretion.
29. FUNCTIONAL SKIN GRAFTS FABRICATED USING A 3D

BIOPRINTER FORM AND MAINTAIN SKIN STRUCTURE AFTER
IN VIVO IMPLANTATION.
Authors: Marco J, Jeong C, Yoo J, Atala A
Medicine
Full-thickness skin wounds and extensive burn injuries are one of
the major causes of morbidity and mortality. Globally, 11 million
burn injuries are reported per year. Between 1998 and 2007, the
overall mortality rate due to burn injuries was 4.9%. Currently, the
clinical standard for wound treatment is the use of autologous
split-thickness skin grafts. Unfortunately, this requires surgery
to remove a portion of the patients skin and is not applicable to
extensive wound coverage. An alternative therapy is the use of
allografts, but immunosuppression is used in conjunction with
this therapy, leading to increased patient susceptibility to illness
and pain.
The application of skin cells onto wound sites to improve wound
healing is a promising area of research. This can provide wound
coverage with minimal skin grafting as cells can be expanded
to cover larger wound areas. Cell printing by a 3D bioprinter
43
Poster Abstracts
has been suggested as a primary form of cell application for
wounded skin or skin grafting to cover such larger wound sites.
The objective of this study was to create functional skin grafts by
printing not only human fibroblasts and keratinocytes but also
human papilla cells for hair follicle formation and human melanocytes for skin pigmentation, all with carefully controlled layering techniques. Fibroblasts and papilla cells were suspended in
a printable hydrogel containing fibrin. These cells were printed
first in order to create the dermal layer. Keratinocytes and melanocytes were suspended in the same hydrogel and were printed
second to create the epidermal layer. The constructs were 1 cm
x 1 cm and only two layers thick in order to mimic the thickness
of normal mouse skin. Once the constructs were printed, they
were cross-linked with thrombin to make the gels stable and
firm. The bilayered skin grafts were cultured for 5 days and then
implanted onto nude mice.
After a week of in vivo implantation, the constructs showed
revascularization and started to mimic the structure of mouse skin.
This indicated that the mice were not rejecting the implanted skin
grafts. The constructs were also able to maintain their structural
integrity during this time and were easily retrieved for analysis.
A gel-only group (used as control) was also implanted on each
mouse along with cell-seeded hydrogels. The gel-only group did
not maintain its structure and was not retrievable after one week.
This indicated that the cells within the construct were producing a
sturdy matrix. Massons Trichrome staining confirmed the presence of ECM in the cell-containing constructs. Finally, it was noted
that the size of the wound containing the cells in hydrogel were
slightly bigger than the gel-only group, indicating that cells from
the surrounding area are not migrating in to close the wound
and suggesting that the construct is being allowed to integrate
into the skin. Further analysis and relevant results from this study
are ongoing. Based on the current data, we conclude that the
constructs are capable of forming and maintaining their skin-like
structure even after 1 week of in vivo implantation (12 days after
printing). Constructs will be retrieved again at 3 weeks in vivo (26
days after printing) in order to examine the structural integrity,
to determine if follicles are being formed, and to ascertain if any
further pigmentation can be seen.
30. SEEDING OF PIG THYMUS SCAFFOLD EX VIVO USING

MOUSE THYMIC EPITHELIAL AND BONE MARROW CELLS TO
REGENERATE A FUNCTIONAL THYMUS
Authors: Singh S, Marco J, Gutierrez S, Jackson J
Medicine
Old age has a detrimental effect on the function of various tissues
and organs in the body, one of which is the thymus. Aging causes
thymic involution, resulting in the loss of structural and functional
abilities of the thymus. The thymus is a specialized organ in the
immune system involved in the maturation of T-cells. It consists
of two lobes, which are further divided into lobules, and each
lobule contains a cortex and a medulla. T cells are produced from
the T cell precursors that are present in the bone marrow. These
progenitor cells enter the thymus and mature as they move
through the different regions of the thymus. With the progression
44
of age, there is a decrease in the amount of circulating nave T

cells, which renders the immune system less effective in fighting
novel infections. One approach to restore the immune system in
aged individuals is the regeneration of the thymus, which is the
objective of this project.
Specifically, the purpose of this study was to analyze the maturation of bone marrow progenitor cells when seeded in a pig thymus scaffold along with mice epithelial cells. First, a pig thymus
was decellularized using a mild detergent in order to remove all
the cellular components and obtain an extracellular matrix scaffold. This scaffold (5 cc) was then seeded with different amounts
(1 million, 2 million, and 5 million) of mice thymic epithelial cells,
and the attachment and survival of these cells in the scaffold was
histologically assessed over three weeks. Next, the scaffold was
seeded with both bone marrow progenitor cells and thymic epithelial cells to evaluate the effect of the association of these two
types of cells on cell attachment and retention in the scaffold. A
flow cytometry analysis was also performed on the cells extracted
from the scaffold to detect maturing T cells, the presence of which
would indicate functional regeneration of the thymus.
Histological analysis of the scaffold seeded with thymic epithelial
cells revealed cell attachment after one week. However, a loss of
cells from the scaffold was observed at the end of the second and
the third weeks. Immunohistochemical staining also suggested
that medullary epithelial cells survived better than cortical cells.
For the second reseeding experiment, samples from the first
week time point have been obtained thus far. Cell attachment
in the scaffold was observed, and the epithelial cells displayed
cell-specific markers, cytokeratin 5 (expressed by medullary cells)
and cytokeratin 8 (expressed by cortical cells). We will continue to
collect data from samples from the next two time points. The data
analysis will help determine whether the reseeded scaffold provides a functional microenvironment for mature T cell production.
31. DETERMINING HOW TRANSCRIPTION FACTOR GCN4

EXPRESSION CHANGES IN LONGLIVED S. CEREVISIAE
AND C. ELEGANS MUTANTS CONTAINING MITOCHONDRIAL
RIBOSOMAL PROTEIN DELETIONS
Authors: Tesfamariam H, McCormick M, Kennedy B
Presenter Institution: The Buck Institute for Research on Aging
In eukaryotic cells, mitochondria are organelles that contain a
separate set of genetic material (mtDNA) independent of the
genome found in the cells nucleus. Mitochondria have their own
ribosomes distinct from the cytosolic ribosomes in the cell, that
specifically translate some but not all of the other mitochondrial
proteins. Previous experiments have determined that certain
deletions in cytosolic large ribosomal proteins (RPL) result in an
increase in lifespan (Steffenet al., 2008; Steffenet al., 2012) and an
upregulation of GCN4 (Steffenet al., 2008). The upregulation of
Gcn4, a nutrient responsive transcription factor, suggests deletions in ribosomal proteins initiate changes in cell metabolism that
ultimately increase lifespan. Therefore, we wanted to determine
whether the lifespan-extending mitochondrial large ribosomal
protein (MRPL) deletions have a similar relationship to Gcn4. The
Poster Abstracts
role of Gcn4 will be analyzed in both the budding yeast Saccharomyces cerevisiae and the nematode C. elegans.
applications, the mechanisms and biological relevance must be

understood as completely as possible.
Our approach to understanding whether any of these novel longlived strains containing an MRPL deletion show an up-regulation
of Gcn4 is based upon a plasmid containing a dual-luciferase
reporter. Firefly luciferase label fused to the GCN4 gene is used
to measure the GCN4 protein expression. The relative amount
of firefly luciferase activity will be compared to Renilla luciferase
fused to Pgk1, a housekeeping protein, which will be used as a
baseline reference. We can measure relative differences in protein
expression levels compared to Pgk1 gene expression. These Gcn4
level measurements will be normalized relative to a wild-type
control strain.
The objective of this study was to ascertain the hormone production of in vitro follicle-like structures in response to gonadotropins. Rat ovarian cells were cultured in a micro-well system for
several days to allow them to form these structures, which were
cultured in either the basal germline stem cell media or in the
same media treated with LH and FSH. These two gonadotropins
are known to stimulate the production of hormones by the ovary
in vivo. The cell growth media was collected every other day and
assessed for the presence of two such hormones, -estradiol
and progesterone using an ELISA. Anti-Mllerian Hormone
(AMH), which is frequently used in conventional fertility treatments as a means for assessing ovarian reserve was also assayed
as an indicator of the same quality of the ovarian follicle-like
structures that we were able to produce. Cells were fixed every
other day and plated onto chamber slides for H&E morphology
analysis and staining of a marker for the zona pellucida, which is
a glycoprotein membrane that surrounds the plasma membrane
of mature oocytes, or egg cells.
A C. elegans model was selected to observe if Gcn4 activity was

conserved in a higher level multicellular organism. C.elegans have
relatively short lives, making them ideal multicellular organisms
on which to conduct lifespan studies. The C. elegans used in this
study will be fed E. coli containing dsRNA producing plasmids to
knockdown the orthologs of the S. cerevisiae mrpl genes by RNAi.
Lifespan of the nematodes will be recorded and standardized
against a wild-type strain to determine if mrpl deletions can
extend lifespan in C. elegans. Conducting this experiment in a
C. elegans model will allow us to determine if mrp also play a role
in C. elegans lifespan. Finally, we will also delete GCN4 in both
S. cerevisiae and C. elegans to determine if Gcn4 is necessary in
both organisms for the observed increase in lifespan. Ultimately,
these studies will allow us to test the conservation of these mechanisms across eukaryotic organisms.
32. IN VITRO GENERATION AND CHARACTERIZATION

OF HORMONE-RELEASING OVARIAN FOLLICULAR
STRUCTURES
Authors: Szymkowiak S, Joo S, Yoo J
Medicine
Ovaries serve two very important functions in the body: hormone
production and reproduction. Loss of ovarian function due to
menopause, polycystic ovarian syndrome, chemotherapy, radiation, or any other cause either natural or induced not only causes
infertility but also causes other hormone-related physiological
complications. While conventional hormone replacement therapy,
in the form of an injection or pill, is able to maintain female
secondary sexual characteristics, this therapy has its own set of
complications and side effects and is unable to restore fertility.
Creation of ovarian tissue that can produce fertile eggs and the
necessary hormones would provide numerous benefits to women
of all ages. The results of this study demonstrate the influence of
luteinizing hormone (LH), follicle-stimulating hormone (FSH), and
interactions between the two on the production of physiologically necessary hormones and the morphological changes that
result from gonadotropin stimulation, which is an important step
in a much bigger project. These methods for growing ovarian cells
in aggregates have been previously demonstrated and characterized, but the hormone profile of the follicle-like structures had
not been established; if this technology is going to have clinical
The results demonstrate a qualitative difference between the

basal cultures and those cultured in the presence of FSH and LH.
The cultures with gonadotropins added display a quicker self-organization into coherent follicle-like structures. Furthermore, the
aggregates grown in the presence of gonadotropins produced
more oocytes, which matured to a higher average diameter than
did the aggregates cultured in basal media. Mature oocytes
with zona pellucida antibody staining were visible in culture
groups after day 3. The cultures with FSH and LH added to them
produce higher levels of both -estradiol and progesterone than
the basal cultures. These results demonstrate that the addition
of the gonadotropins LH and FSH stimulates the development of
the follicle-like structures, and their ability to produce hormones,
as predicted.
33. RESCUE OF MITOCHONDRIAL DYSFUNCTION BY

TRANSFERRING MITOCHONDRIAL DNA-ENCODED GENES
TO THE NUCLEUS
Authors: Wang S, Crampton A, Powers K, Vanhoozer S,
Boominathan A, OConnor M
Mitochondria serve as the energy source in all eukaryotic organisms. The majority of proteins in the organelle are encoded by
the nuclear genome and transported into mitochondria, and
13 of them are encoded by mitochondrial DNA (mtDNA). Since
mitochondria do not possess a substantial DNA repair system,
mitochondrial DNA mutations accumulate over time can lead to
respiratory chain defects, which can cause insufficient energy
production. Currently, researchers are trying to develop gene
therapies in order to treat human diseases caused by mitochondrial DNA mutations, but available methods are limited. One
approach to treating mitochondrial dysfunction involves inserting
the wild-type copy of a gene normally found in the mitochondria
into the nucleus. The protein can be translated in the cytosol
and targeted to the mitochondria and, therefore, rescue the
45
Poster Abstracts
missing mitochondrial function. Specifically, the recoded mRNA is
exported from the nucleus into the cytoplasm where it is translated while attached to the mitochondrial outer membrane, and
co-translationally imported into the mitochondria. Our present
studies focus on ATP8, which is part of subunit FO in complex V
in the respiratory chain. Previous data from our group showed
that attaching a mitochondrial target sequence (MTS) upstream
to the recoded gene for ATP8 allowed successful expression of
its corresponding protein in Atp8 null cell line. The protein was
efficiently targeted to mitochondria and localized to Complex V;
however, it failed to rescue its function. Here, we discuss strategies to improve functional rescue i.e., optimizing the MTS, and by
attaching a 3UTR downstream to the gene.
34. ARE EXTRACELLULAR VESICLES AN ECONOMICALLY

FEASIBLE ALTERNATIVE TO CELL-BASED THERAPEUTICS?
Authors: Smith J3, Ng K1-3, Mead B1-3, Reeve B3, Brindley D3-6, Karp
M1-3
Division of Biomedical Engineering, Department of Medicine,
Center for Regenerative Therapeutics, Brigham and Womens
Hospital, Harvard Medical School
2
Harvard-MIT Division of Health Sciences and Technology
3
Harvard Stem Cell Institute
4
The Oxford-UCL Centre for the Advancement of Sustainable
Medical Innovation, University of Oxford
5
Nuffield Department of Orthopaedics, Rheumatology and
Musculoskeletal Sciences, Nuffield Orthopaedic Centre, University
of Oxford
6
Centre for Behavioural Medicine, UCL School of Pharmacy,
University College London
This study examines the economics of biomanufacturing processes for therapeutic cells in comparison to extracellular vesicles
(EVs) that such cells produce. Cells constitutively secrete EVs that
harbor an array of biomolecules including mRNA, microRNA
and proteins. Increasing evidence indicates that EVs secreted by
therapeutic cells can effect similar benefits to cells themselves,
suggesting that EV therapy could serve as a potential alternative
to cell therapy. There are several reasons why EV therapy may be
advantageous. For example, compared to the dynamic nature of
cells and their varied responses to the local microenvironment,
EVs are relatively stable. In particular, EV therapy obviates the
inherent risk of tumorigenesis that accompanies cell therapy, such
as therapeutic use of embryonic stem cells and their progeny.
From a regulatory perspective, EVs may be more specifically
defined biochemically, which could alleviate some difficulties of
quality control associated with cell therapy. Given the high costs
of developing new therapeutics, analysis of economic feasibility
and scalability early in the developmental pipeline is important.
Therefore, we are designing bioprocess models for EV production
based on existing cell therapy production processes with the
eventual aim of analyzing the cost of goods for various cell/EV
doses and production processes. This work is critical in evaluating
the potential of EV treatment to reach the clinic on a larger scale
and will serve as a useful reference for commercial and academic
parties looking to develop EV-based therapies and products.
46
35. MANUFACTURING REQUIREMENTS FOR TRANSLATING

HOLLOW ORGAN TISSUE ENGINEERING TO ROUTINE
CLINICAL PRACTICE
Authors: Jones R1, Brindley D2,3, Birchall M4, Wall I1,5
UCL Department of Biochemical Engineering
2
Botnar Institute of Musculoskeletal Sciences, Nuffield Department
of Orthapaedics, Rheumatology and Musculoskeletal Sciences,
University of Oxford
3
The Oxford-UCL Centre for the Advancement of Sustainable
Medical Innovation, University of Oxford
4
UCL Ear Institute, University College London
5
Department of Nanobiomedical Science, BK21 PLUS NBM Global
Research Center for Regenerative Medicine, Dankook University
Clinical success of transplanting bioengineered hollow organs has

already been achieved: bioengineered tracheas being the most
prominent example. Although many different approaches have
been taken, results have been varied, and currently there is no
clear consensus regarding the gold standard method to produce
the bioengineered transplants.
In response to this gap in the field, we have carried out a detailed
review of methods used so far, looking at each stage of production, from creation or harvest of the scaffold to transplantation
into the recipient patient. Current protocols have been assessed,
bioprocessing bottlenecks of each stage in production have been
identified, and potential solutions have been suggested where
possible. Key translational challenges from a non-manufacturing
perspective have also been acknowledged. It is hoped that by
addressing these issues clinical adoption of tissue-engineered
organs will become more widespread.
Process maps for each stage of production have been created.
In terms of the scaffold, we have focused on methodologies
that employ decellularization as they present native extracellular matrix, although it has been widely suggested that future
scaffolds might combine both natural and synthetic components,
yielding the desired biological and mechanical properties.
Bioactive molecules and their documented effect on tissue-engineered transplants have also been assessed. A table of candidate
regenerative growth factors has been created to evaluate the
potential of each option, to reflect that to date there is still no
clear consensus regarding the optimal combination of molecules
and their quantities.
Objectives for bioreactor design have been identified and
assessed. GLP certified hollow organ bioreactors have already
become commercially available, yet there is still widespread
desire for greater automation in current designs with respect to
control and monitoring of process and product. However, before
this can be achieved, operating parameters themselves need to
be defined. For example, there is currently no published information as to the optimum pH at which these engineered constructs
should be held during the seeding and culture process. Furthermore, current seeding via micro-syringe needs to be modified to
Poster Abstracts
reduce contamination risk, increase reproducibility, and widen
availability of this technology.
Finally, this review has identified the currently available production methods that are the most promising candidates to
achieve standardized manufacture, whilst indicating where future
improvements can be made, particularly regarding quality assurance and quality control in the manufacture of bioengineered
hollow organs. With clinical trials for bioengineered tracheas
already underway, it is time for focus to shift to the long-term
biomanufacturing strategy of these organs. This will ultimately
ensure that the best quality tissue-engineered organs are being
produced through safe and monitored protocols, where there
is potential for scale-up and widespread clinical adoption of this
technology.
36. DETERMINING THE IMPACT OF HOMOLOGOUS

RECOMBINATION INHIBITORS ON THE ALT CANCER
PATHWAY USING A HIGH-THROUGHPUT AND HIGHCONTENT VERSION OF THE APB ASSAY
Authors: Wu C, Silva H
In normal cells, telomeres shorten progressively with each cell
division, inducing cellular senescence and apoptosis. In cancer
cells, however, cells use telomere maintenance mechanisms
(TMM) allowing for unlimited proliferation and tumorigenesis. It is estimated that 10-15% of cancers use the Alternative
Lengthening of Telomeres (ALT) pathway, a proposed mechanism cancer cells activate when the commonly studied telomerase pathway is absent. The purpose of this project is to (1) to
optimize one of the few available ALT-specific assays (the APB
assay), for high-throughput screening and (2) to perform a pilot
drug screen to assess the potential of specific drugs for ALT
cancer therapy.
Unlike the telomerase-based pathway, much of the ALT pathways molecular mechanism is still unknown. Yet, of what is
known, ALT relies primarily on the homologous recombination
(HR) machinery and is correlated with at least one or more of the
following three markers: (1) long and highly heterogeneous telomere length, (2) the presence of C-circles, and (3) the presence
of ALT-associated promyelocytic nuclear bodies (APBs). C-circles
are extrachromosomal telomeric repeats of partially double-stranded, C-rich (CCCTAAA) circles. These circular telomeric
DNA pieces can be detected by rolling circle amplification, which
generates long strands of complementary TTAGGG repeats
(C-circle assay). While the presence of C-circles measured via the
C-circle assay has been validated as a positive marker for virtually
all known ALT-positive cell lines, this project focuses on the APB
assay and furthering the understanding of its usefulness as an
ALT marker in a high-throughput, high-content screen. In this
assay, we identify APBs by the co-localization of fluorescently
stained telomeric chromatin (i.e. TRF2) within promyelocytic
(PML) nuclear bodies in cell nuclei.
My summer project first involved optimizing the APB assay to
provide a standard protocol for cell culture, image acquisition,
and analysis in a high-throughput format. We used a model drug,

hydroxyurea, to optimize experimental parameters. Using the
optimized APB assay, I ran a pilot drug screen using four drugs
identified as HR inhibitors that target the RAD51/RecA protein
family. RAD51 and its homolog RecA play a major role in HR
during double-strand break repair by binding to DNA at the site
of a break and covering it in a protein sheath as the first step
of the HR pathway. As ALT is hypothesized as a HR-dependent
process using either linear or circular telomeric templates, we
analyzed the potential effect of these drugs on ALT with our
high-throughput and high-content APB assay. We analyzed
the data resulting from the APB assay with several parameters
in mind, all of which provide us further understanding of drug
action mechanisms and the functional impact anti-HR drugs
have on the ALT pathway. In particular, we quantified the
number of APBs to measure ALT activity; the total cell count to
determine drug toxicity or cell cycle arrest, which was measured
further by area and intensity of nuclear staining; and the area
and intensity of the APB, PML, and TRF2 foci. This pilot drug
screening demonstrates that our APB assay is a valid method
for high-throughput drug screens and reveals one drug as a
potential inhibitor of ALT activity.
37. IDENTIFICATION OF SCARA5, A NOVEL BIOMARKER IN

BONE PATHOPHYSIOLOGY
Authors: Zada S, Hurley H, Brindley D, Al-Mossawi H, Sabokbar A
Presenter Institution: University of Oxford
As the human body succumbs to aging, the natural effect of
deterioration takes place. Homeostatic mechanisms in the bone
falter as bone resorption surpasses bone synthesis. A reduction
of bone density takes place, which results in shorter stature and
a curved posture. Early onset of this aging effect can also occur
in diseased joints, producing debilitating aches and pains. The
causes of bone diseases such as osteoarthritis and rheumatoid
arthritis are currently unknown. Therefore, unfortunately, prevention is not available as a therapeutic option.
In the Sabokbar Lab at the University of Oxford, the scavenger
class A receptor member 5 (SCARA-5) is being studied for its
prospective role in ameliorating the mechanisms behind bone
disease. Results from past transgenic studies present SCARA-5
functioning through osteoblasts. Therefore, in SCARA-5 knockout samples, the lack of this critical bone remodeling protein
results in a loss of osteoblast regulation. This caused increased
trabecular and cortical bone density in mice femurs.
In previous cell culture experiments, murine osteoblast and
osteocyte-like cell lines were used to demonstrate the effects of
SCARA-5 in vitro. For the murine animal model, a recombinant
murine SCARA-5 protein (m-SCARA5) was used in the in vitro
studies. Cell proliferation, alkaline-phosphatase (ALP) activity,
and mineralization assays were performed to study cellular
behavior in the presence of exogenous additions of m-SCARA5.
Quantitative RT-PCR was used to assess the SCARA-5 mRNA levels and other critical bone remodeling proteins. These proteins
were of interest in the investigation of the mechanism behind
SCARA-5s activity.
47
Poster Abstracts
In the cell culture assays, the results via the cell proliferation
and ALP assays indicated that m-SCARA5 inhibits osteoblast
differentiation and activity. In contrast, mineralization detection
and qRT-PCR results show SCARA-5 expression had insignificant
effects on osteoblast-dependent mineralization. However, these
inconsistent results may be due to in-vitro experiments being
incapable of adequately portraying the in-vivo microenvironment. Therefore, experiments on osteoclasts in human diseased
tissues will be performed to configure SCARA-5s mechanism in
bone remodeling and its diseased counter state.
Osteoarthritic and rheumatoid arthritic human tissue samples
will be used to compare SCARA-5 expression in diseased and
normal cells. Immunohistochemistry using an anti-SCARA-5
antibody can reveal such expression. H&E staining of these tissue
sections will allow for the visualization of the multi-nucleated
osteoclasts. From these osteoclast numbers, the importance of
SCARA-5 in bone remodeling can be assessed. It is reasonable
to postulate that SCARA-5 expression in the human system, or
lack thereof, will produce results corroborated by the previous
murine experiments. The goal of this project is to conclusively
define a significant differential SCARA-5 expression between
diseased and normal tissue.
38. META-ANALYSIS LEADS TO DEEPER UNDERSTANDING

OF CELLULAR SENESCENCE
Authors: Morrissey C, Mooney S
Presenter Institutions: The Buck institute on Aging Research
In the 1960s it was discovered that healthy cells could not proliferate in vitro indefinitely. After some maximum number of cell
divisions the cells, while still viable, would no longer undergo
mitosis and would transition to a senescent state. This senescent
state has long been believed to play a role in aging as senescent cells accumulate in older tissues. More recently this link
has been strengthened through the discovery of a set of extra
cellular signal proteins secreted by senescent cells which have
been shown to play a role in chronic inflammation associated
with aging. Senescence has also long been believed to be an
anti-cancer mechanism as this cellular state can be triggered by
certain oncogenes, and it is a direct check against the rampant proliferation necessary to form tumors. The relationship
between senescence and cancer has been complicated by more
recent findings that the secreted signal protein cohort characteristic of senescent cells can be conducive to tumor growth in
the surrounding tissue. Further complicating our understanding
of this cell fate, senescent cells have also been found to play
a beneficial role in wound healing in healthy tissues, and a
deleterious role in tissues with a high burden of senescent cells.
This unique set of beneficial as well as harmful effects for the
organism, leads us to believe that cellular senescence is a potential example of antagonistic pleiotropy wherein the evolutionary advantage senescence provides as a check against cancer
and an aid in wound healing outweighs its deleterious effects
one older, post reproductive organisms. As such it provides an
attractive target for therapeutic regulation.
48
We aim to better understand these myriad aspects of cellular

senescence by conducting a meta analysis of available data
for various models of senescence in both mouse and human
tissues. It is already understood that senescence can be induced
by a number of factors including telomere shortening, DNA
damage, and the expression of certain oncogenes. Despite the
mode by which senescence is induced, there are some characteristic changes in gene expression that seem to be cell type
independent, and conserved between mouse and human. Still,
the mechanisms by which cells transition to the senescent state
are not fully characterized. We are integrating transcriptomic,
proteomic, and epigenetic data from a number of studies to
better understand these signatures of senescence. We hope
to leverage the available gene ontologies and annotations to
interrogate the network of gene pathways involved with this
fascinating cellular state.
Initial results indicate that we are able to detect transcriptional
regulation of the genes involved with the senescence-associated
secretory phenotype as well as genes involved in mitotic replication. Gene set enrichment analysis has also indicated changes to
the lysosome may accompany this cell fate. As the core pathways
for induction of senescence are illuminated, we hope to utilize
tools like the connectivity map, cmap, and the small molecule
pathway database to identify druggable windows into the regulation of this complex process.
Notes
49
Notes
50
About the
At SENS Research Foundation (SRF), we believe that a world free

of age-related disease is possible. Thats why were funding work
at universities across the world and at our own Research Center in
Mountain View, CA.
Our research emphasizes the application of regenerative medicine to

age-related disease, with the intent of repairing underlying damage
to the bodys tissues, cells, and molecules. Our goal is to help build
the industry that will cure the diseases of aging.
SRF is, at its core, a research-focused outreach organization. Our

outreach efforts include the biennial SENS conference at Cambridge,
speaking engagements, and general advocacy. We strive to inform
policymakers and the public at large about the promise of the
damage-repair approach to treating age-related disease.
sens research foundation - 110 Pioneer Way, Suite J - Mountain View, CA 94041 - USA
phone: 650-336-1780 - fax: 650-336-1781
www.sens.org
51
We would like to thank our conference sponsors:
Gold Sponsor
Silver Sponsors
Bronze Sponsors
Supporting Sponsors
Media Sponsor

Rejuvenation Biotechnology 2014 Full Program

Hochgeladen von

Dokumentinformationen

Copyright

Verfügbare Formate

Dieses Dokument teilen

Dokument teilen oder einbetten

Freigabeoptionen

Stufen Sie dieses Dokument als nützlich ein?

Sind diese Inhalte unangemessen?

Copyright:

Verfügbare Formate

Rejuvenation Biotechnology 2014 Full Program

Hochgeladen von

Copyright:

Verfügbare Formate

August 21-23, 2014

Santa Clara, California

a SENS Research Foundation Conference

a SENS Research Foundation Conference

August 21-23, 2014

Registration in LOBBY WEST

Registration (until 5:00 pm) - [LOBBY WEST]

Networking Breakfast - [Ballrooms EFGH]

Technologies for Reversal of Aging - [Ballrooms ABCD]

Networking Lunch & Exhibits - [Ballrooms EFGH]

CONCURRENT SESSIONS. PLEASE CHOOSE ONE:

Alzheimers Disease Session 1

Cardiovascular Disease Session 1

This session will highlight two types of

Building upon the idea discussed by the

Jean Hbert, Professor, Departments of

Immunotherapy and Imaging

Claude Wischik, Professor of Old Age

Guillermo Garcia Cardena, Associate

David Brindley, Research Fellow,

University of Oxford/Center for the

Neil Littman, Business Development

James ONeill, Partner and

Chief Operating Officer, Mithril

Bernard Siegel, Executive Director,

Michael West, CEO, BioTime, Inc.

CONCURRENT SESSIONS. PLEASE CHOOSE ONE:

Alzheimers Disease Session 2

Cardiovascular Disease Session 2

A third type of damage being targeted for

In this session, examples of current

Ashley Bush, Head of the Oxidation

Research Institute, University of

Rachelle Doody, Professor of Neurology,

and Alzheimers Disease: What are We

Eric Siemers, Medical Director,

Gabor Forgacs, Professor, Biophysics

Laboratory, Department of Physics

Linda Marban, CEO, Capricor

Tissue Engineering Solutions for

David Brindley, Research Fellow,

University of Oxford/Center for the

Catalina Hoffman, Founder, Catalina

Peter Nakada, Managing Director of Risk

Afternoon Break & Exhibits - [Ballrooms EFGH]

Aubrey de Grey, CSO, SENS Research Foundation: (Moderator)

Poster Session/ Buffet Dinner & Exhibits - [Ballrooms EFGH]

Performance by Comedian Hal Sparks - [Ballrooms ABCD]

Registration (until 5:00 pm) - [LOBBY WEST]

Networking Breakfast & Exhibits - [Ballrooms EFGH]

Opening Remarks by Edward James Olmos, Actor - [Ballrooms ABCD]

Toward a New Research Paradigm Panel - [Ballrooms ABCD]

Networking Lunch & Exhibits - [Ballrooms EFGH]

CONCURRENT SESSIONS. PLEASE CHOOSE ONE:

Parkinsons Disease Session

This session will highlight current breakthroughs in cancer research. Additionally,

This session will feature the latest in

Judith Campisi, Professor, Buck Institute

Julie Andersen, Professor, Buck Institute

Laura Esserman, Professor, Departments

Jeanne Loring, Professor, Scripps

of Surgery and Radiology, and Affiliate

Accelerating Knowledge Turns: The

Dale Schenk, CEO, Prothena