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Isoenzyme Inhibited By Cigarette Smoke
May Have Role In Aging And Neurodegeneration
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WESTPORT, Oct 07 (Reuters) - The bulk of research suggests that cigarette
smoke inhibits the activity of monoamine oxidase B (MAOB).

Researchers show, in the October issue of Nature Genetics, that this
inhibition may lead to a rise in cerebral levels of phenylethylamine (PEA),
a neuroactive compound linked to schizophrenia and other psychiatric
disorders.

Dr. Jean C. Shih of the University of Southern California in Los Angeles
and a multicenter team knocked out the gene for MAOB in a group of mice.
The mice exhibited increased levels of PEA, but not of serotonin,
norepinephrine or dopamine, which are also regulated by the monoamine
oxidases.

MAOB-deficient mice also demonstrated an "...increased reactivity to
stress," consistent with the demonstrated role of PEA "...in modulating
mood and affect."

"In addition," the scientists report, "...mutant mice were resistant to the
neurodegenerative effects of MPTP, a toxin that induces a condition
reminiscent of Parkinson's disease." This finding "...demonstrates
unequivocally that MAOB is required for MPTP toxicity," suggesting a role
for the isoenzyme in the aging process.

Dr. Shih and colleagues explain that the findings indicate a "...primary
role for monoamine oxidase B in the metabolism of phenylethylamine."

Moreover, "Because MAOB may promote the aging process in the brain...
MAOB-deficient mice may be useful in studying mechanisms of neuroprotection
and aging."


Nat Gen 1997;17:206-210.
Westport Newsroom 203 319 2700
Copyright 1997 Reuters Limited.
<http://www.reutershealth.com/news/docs/199710/19971007scb.html>
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