Schizophrenia
Articles
Gene increases
schizophrenia risk, says study
First risk gene for schizophrenia found in the general
population
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by Jessica Whiteside
University
of Toronto
Nov. 12, 2002 -- Scientists at U of T have discovered
the first "risk gene" for schizophrenia found
in the general population.
An uncommon variation of a gene called Nogo, when
inherited from both parents, increases the risk of
developing schizophrenia, says a study to be published
in Molecular Brain Research Nov. 15. Previous findings
about other risk genes for the disease were restricted
to specific ethnic groups.
"Finding a risk gene in the general population -
the first finding of this type internationally - opens
the door to discovering new and related risk genes. Now
scientists will know where to look for related
genes," says pharmacology and psychiatry professor
Philip Seeman. "This will help in diagnosis and
potentially in the design of new medications for
treatment of this terrible disease," adds Seeman
who worked on the study with psychiatry professor Teresa
Tallerico, lead author and pharmacology graduate student
Gabriela Novak and undergraduate student David Kim.
The study shows that one in five people with
schizophrenia has this risk gene. Researchers found that
17 of 81 individuals with schizophrenia - 21 per cent -
had inherited the uncommon Nogo variant gene from both
parents. In a control group of individuals without
schizophrenia, only three per cent had inherited the
gene from both parents. People can inherit the variant
Nogo gene from just one parent but there's a
schizophrenia risk only when this gene is inherited from
both parents. The gene does not suggest a diagnosis for
schizophrenia but rather an increased predisposition to
the illness.
One of the Nogo gene's functions is to produce proteins
that inhibit the growth of nerve endings in the brain.
Unlike the common form of Nogo, the variant gene has
three extra chemical bases, known as CAA, in a region of
the gene that regulates protein production. The
researchers found that activity of the Nogo genes was
higher in the post-mortem brain samples of individuals
with schizophrenia. It is possible that these extra CAA
bases lead the variant Nogo gene to produce more
proteins, thereby reducing the number of nerve endings
in regions of the brain associated with schizophrenia
symptoms, Seeman says. However, more research is needed
to confirm this.
"This study adds to the rapidly evolving theory
that, in the brain of those who suffer from
schizophrenia, the nervous system develops in a slightly
altered fashion leading to the onset of symptoms such as
hallucinations and delusions in young adulthood,"
says Seeman.
Although the cause of schizophrenia is not known, the
treatment of the symptoms has been well-established
since the 1970s. Antipsychotic medication is used to
block the action of dopamine, an adrenaline-like
chemical transmitter in the nervous system that becomes
overactive in people with schizophrenia.
"This finding of a risk gene in the general
population could lead to the development of medications
outside the dopamine system, perhaps targeting the
protein produced by the gene," suggests Seeman.
The study was supported by the National Alliance for
Research on Schizophrenia and Depression, the Eli Lilly
Research Fellowship in Women's Mental Health, the
Stanley Foundation Scholars Mentors Program of the
National Alliance for the Mentally Ill, the Canadian
Institutes for Health Research, the Ontario Mental
Health Foundation and the National Institute on Drug
Abuse. Professor Tallerico is an Essel Investigator of
the National Alliance for Research on Schizophrenia and
Depression (NARSAD) and Professor Seeman is a Janice
Lieber Investigator of NARSAD.
Jessica Whiteside is a news services officer with the
department of public affairs
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