|
Genes
May Play Role in Schizophrenia
NEW
YORK (Reuters Health) - Although the causes of the complex psychiatric
disorder schizophrenia remain elusive, new research is uncovering
some of the fundamental mechanisms that seem to steer schizophrenics'
brains down the wrong path.
Experts believe
that genes, developmental factors and environment act in concert
to trigger schizophrenia, but how and why are unknown. In two
new studies, researchers have discovered potential answers to
the question of ``how.''
One study
links schizophrenia to the activity of genes affecting the formation
of nerve fibers in the brain during a crucial time of life--late
teens and early adulthood.
The other
suggests that reactivation of normally harmless, body-dwelling
viruses may trigger the onset of the disorder in some people.
Findings from
both studies are published in the April 10th issue of Proceedings
of the National Academy of Sciences.
Schizophrenia
is a chronic, severe brain disorder that affects about 1% of the
world's population. It profoundly alters an individual's perceptions
of reality, thought processes and emotions. Symptoms typically
surface during the late teens and 20s, and this fact has led many
scientists to focus on early development for clues to what goes
wrong in the schizophrenic brain.
In one of
the new studies, which looked at 35 schizophrenics, researchers
found that spinal fluid from 29% had signs of particular retroviruses
that normally lie dormant in the body. In contrast, the viruses
did not show up in spinal fluid taken from a group of people who
were either healthy or had a brain disorder other than schizophrenia.
The retroviruses--a
group called human endogenous retroviral-W (HERV-W)--are unlike
HIV and other retroviruses in that they are part of the human
genetic makeup. During evolution, the viral genes were incorporated
into human DNA, where they apparently live in peace.
But, Dr. E.
Fuller Torrey told Reuters Health, these viral genes are not the
``junk'' genetic code scientists once assumed they were. In fact,
these findings suggest that HERV-W retroviruses may become involved
in the disease process if they are activated. What might activate
them is unclear, according to Torrey, of the National Alliance
for the Mentally Ill Research Institute in Bethesda, Maryland.
It is possible,
Torrey said, that an outside virus might ''turn on'' HERV-W viruses
and initiate a series of chemical reactions that lead to schizophrenia
in some people. This activation, according to Torrey, might happen
early in life, but it could also occur later.
``If we're
correct that HERV-W becomes activated, and we find out what's
turning it on,'' he said, ``then we may be able to interfere with
what turns it on.''
In the second
study, researchers led by Dr. Allen A. Fienberg of Rockefeller
University in New York City found that schizophrenics have low
activity in five genes that help generate myelin, the protective
sheath that surrounds nerves. Using autopsied brain tissue from
12 schizophrenics and 12 non-schizophrenics, Fienberg's team found
that 89 genes differed in expression between the two groups. Only
the five myelin genes were underactive in schizophrenics.
Disrupted
myelin formation may underlie the brain abnormalities seen in
schizophrenia, according to Fienberg and his colleagues. This
idea, they note, is consistent with the fact that myelin formation
in the brain's prefrontal cortex has been found to occur in the
late teens and early adulthood--when schizophrenia usually arises.
Neither of
these studies point to the root cause of schizophrenia, but, Torrey
said, ``none of us pretends there is one cause for schizophrenia.''
It is ``quite
possible,'' he noted, that his team's findings apply only to a
subgroup of schizophrenics.
Retroviruses
may be related to schizophrenia in some people, but much more
research is needed to confirm that, Dr. David Lewis of the University
of Pittsburgh Medical Center in Pennsylvania told Reuters Health.
``It is almost
certain that the brains of individuals with schizophrenia have
a number of abnormalities,'' he explained. ''Some may represent
causes of the diseases--which may differ across individuals--some
may be the consequences of those causes, and some may be...the
brain's response to try to restore normal function.''
Making these
distinctions, Lewis said, is one of the major challenges in schizophrenia
research.
SOURCE:
Proceedings of the National Academy of Sciences 2001;98:4634
Reference
Source 89
For more information on how to prevent other diseases, use
PreventDisease.com's "Quick
Prevention Resources".
|
