Activity of brain enzyme targeted by mood stabilizing drugs appears to be decreased in brains of teenagers who die by suicide
The activity of a key enzyme linked to mood
disorders and the action of some mood stabilizing drugs appears
to be decreased in the brains of teenagers who die by suicide, according
to an article in the July issue of the Archives of General Psychiatry.
According to the article, approximately 30,000
people die of suicide in the United States annually, with suicide
the second leading cause of death among teenagers. Although there
is some understanding about the psychological and psychosocial factors
associated with teenage suicide, little is known about neurobiological
factors that may contribute to teenage suicide. The enzyme called
protein kinase C has been linked with mood disorders, and it is
the target of some mood-stabilizing drugs.
Ghanshyam N. Pandey, Ph.D., and his American
colleagues investigated whether there was any link between changes
in enzyme activity and teenage suicide by examining the brains of
17 teenage suicide victims and brains of 17 teenagers without psychiatric
illness who did not commit suicide.
Of the 17 suicide victims, 9 had a history
of mental disorders and 8 had no history of mental disorders, although
2 had a history of alcohol or drug abuse. There were 16 males and
1 female in the control group; among the suicide victims, 10 were
male and 7 were female.
The researchers found that protein kinase
C activity was statistically significantly decreased in certain
brain areas in teenage suicide victims' brains compared with the
brains of control subjects.
"Because many physiologic functions are
mediated through protein kinase C activity and because protein kinase
C is a target for the therapeutic action of psychoactive drugs,
our findings indicate that the pathogenesis of teenage suicide may
be associated with abnormalities on protein kinase C and that protein
kinase C may be a target for therapeutic intervention in patients
with suicidal behaviors," the authors wrote.
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