For Patients

Aging Begins at 30

Progress in Treating Dementia

Ian Maclean Smith, M.D.
Emeritus Professor
Department of Internal Medicine
University of Iowa Hospitals and Clinics
Creation Date: April 2003
Last Revision Date: April 2003
Peer Review Status: Internally Peer Reviewed

Senility as a diagnosis has been replaced by dementia, which is a disease that needs
treatment. Bit by bit we are learning enough of the biochemical and physical or
anatomical characteristics of dementia to have some clues that may help in treatment and
prevention. Biochemical study makes possible blockage of abnormal processes or
providing something missing. Dementia treatment is now entering this exciting stage.
Drs. Ritchie (Montpellier) and Lovestone (London) review new dementia treatments in
the November 30th 2002 Lancet. Dementia is a decline in memory and learning.
Neurological findings and available tests can differentiate different types of dementia,
such as early and late onset Alzheimer's disease, vascular dementia (stroke associated),
Lewy body dementia (with Parkinsonism, visual hallucinations and fluctuating
confusion).
Dementia is diagnosed in 1.5 percent of persons aged 65 and increases to about 30
percent at 80. Average survival, (depending on cause and severity) from diagnosis is 8
years. Possibly 30 percent of the dementias have damaged brain blood vessels due to high
blood pressure and cholesterol with associated blood vessel disease (hardening).
The use of the CAT scan and MRI defines subgroups of dementia, as do various
psychological tests for delayed free recall, verbal fluency and spatial organization.
Special MRI testing is now available in research hospitals to detect biochemical brain
changes.
Dementia risks include age, having a demented close family relative and having an E4
Allele of the APOE gene. Dementia risk is increased in women, persons with herpes, low
blood lipids, prior head injury and exposed to certain anesthetic agents. Diabetes and
excessive alcohol also predispose to dementia. Education beyond high school level and
certain anti-inflammatory drugs such as aspirin and its cousins, appear to be protective,
for uncertain reasons.

Abnormal amounts of protein accumulate in the wrong places such as synuclein (in Lewy
body dementia), tau protein in frontal lobe dementia and Alzheimer's, and amyloid
protein in Alzheimer's. Enzymes involved in these excess accumulations can be blocked.
Cholinergic functions (acetylcholine is a neuromessenger) are lost early in Alzheimer's.
This has led to the use of inhibitors to delay the action of the enzyme that normally
destroys unused choline. About a fifth of Alzheimer's treated patients are benefited.
Molecular studies led to an understanding of the formation of extracellular plaques (flat
patches) and intercellular neurofibrillary tangles, autopsy markers of Alzheimer's. The
plaque is an accumulation of amino acid protein precursors called A-Beta. The gene for
this is on chromosome 21. Immunological treatment in Alzheimer model mice can reduce
plaque formation. Trials in humans were stopped due to side effects.
Neurofibrillary tangles, the second microscopic characteristic of Alzheimer's, are
clumped tau proteins needed for information transfer. Inhibition of the enzyme 6SK-3,
that regulates tau formation, is a treatment to be investigated. Genes on chromosomes 10,
12 and 9 are associated with Alzheimer's and may lead to other treatments.
There are many compounds that show promise for Alzheimer's treatment. There are clues
that anti-inflammatory drugs, (NSAIDs), vitamin E or Vitamin B 12 may help. All these
possible treatments need testing ultimately in a randomized, double blinded trial with
careful measurements of all the signs and symptoms. Behavior disorders are targets for
treatment with established psychiatric drugs but careful evaluation is necessary for their
use in dementia.
To lessen caregiver burden, established psychiatric drugs can control apathy, depression,
delusions and eating disorders. Serotonin reuptake inhibitors (SSRIs) are used to treat
dementia-associated depressions, since they do not interfere with the treatment of
cholinergic problems. Caregiver training is helpful as is respite relief. Detection and
prevention of elder abuse in dementia care has progressed. Studies of when it is best to
institutionalize the demented elderly are in progress.
Hope is on the horizon for the treatment of the unfortunate elderly who suffer from
dementia.
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All contents copyright 1992-2003 the Author(s) and The University of Iowa. All rights reserved.
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