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Both De Bellis and Tapert observed that future studies will need to determine if a smaller
prefrontal cortex represents a vulnerability to, or a consequence of, early-onset drinking.
"It may be that the adolescent prefrontal cortex is more vulnerable than the adult brain to the
negative effects of drinking," said De Bellis. "Or prefrontal-cortex maturation may be impeded by
the neurotoxic effects of substances on the adolescent brain. Another explanation for the smaller
prefrontal cortex and prefrontal-cortex white-matter volumes of adolescents and young adults with
an adolescent onset AUD is an inherent vulnerability for delayed prefrontal cortex maturation that
enhances the risk for poorer executive cognitive functioning and adolescent substance-use
disorders."
"In addition," said Tapert, "we need to figure out the role of the other mental illnesses in these
brain-size abnormalities."
De Bellis and his colleagues are currently examining both brain and cognitive function in
adolescents with substance-abuse problems. "We are very interested in studying if adolescent
brain and cognitive development normalizes after a time period of sobriety," he said.
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Alcoholism: Clinical & Experimental Research (ACER) is the official journal of the Research
Society on Alcoholism and the International Society for Biomedical Research on Alcoholism. Coauthors of the ACER paper, "Prefrontal Cortex, Thalamus and Cerebellar Volumes in Adolescents
and Young Adults with Adolescent Onset Alcohol Use Disorders and Co-Morbid Mental
Disorders," were: Anandhi Narasimhan of Duke University Medical Center; and Dawn L. Thatcher,
Matcheri S. Keshavan and Paul Soloff of the University of Pittsburgh Medical Center. The study
was funded by the National Institute on Alcohol Abuse and Alcoholism.