Sunday, November 14, 2004

Bipolar Disorder, Schizophrenia Key Found

Stress-Activated Molecule Triggers Mental Disturbance

By Daniel DeNoon, WebMD Medical News
Reviewed by Brunilda Nazario, MD
on Thursday, October 28, 2004

Oct. 28, 2004 -- A stress-activated molecule underlies many of the
symptoms of some mental illnesses, a new study shows.

We control our behaviors, thoughts, and emotions via an important part
of the brain: the prefrontal cortex. People with injuries to this part
of the brain become impulsive, distractible, and have poor judgment.
Major damage to the prefrontal cortex can cause thought disorders and
hallucinations.

These symptoms are also seen in people with bipolar disorder and with
schizophrenia. These mental illnesses worsen with stress.

Recent studies also link worsening bipolar disorder and schizophrenia
with changes in brain signaling by a molecule called protein kinase C
or PKC.

In rat and monkey studies, Yale researcher Amy Arnsten, PhD, and
colleagues delivered PKC directly to the prefrontal cortex of rats and
monkeys. Sure enough, PKC impaired the animals' mental functioning.

Drugs that block PKC restored mental functioning. Some of these drugs
include medicines commonly used to treat mental illness, such as
lithium and valproate.

Arnsten and colleagues report their findings in the Oct. 29 issue of
Science.

"Excessive PKC activation can disrupt... regulation of behavior and
thought, possibly contributing to signs of prefrontal cortical
dysfunction such as distractibility, impaired judgment, impulsivity,
and thought disorder," Arnsten and colleagues write.

It's possible that new drugs with improved PKC-blocking activity could
lead to better treatment of bipolar disorder, schizophrenia, and
perhaps other mental illnesses.

Interestingly, PKC plays a role in lead poisoning. The findings,
Arnsten says, could lead to a better understanding of the symptoms of
distractibility and impulsivity seen in children with lead poisoning.

SOURCES: Birnbaum, S.G. Science, Oct. 29, 2004; vol 306: pp
882-884. News release, Yale University.

No comments: