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February 2011



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Article Date: 03 Feb 2011 – 3:00 PST

In a major advance for schizophrenia research, an international team of scientists, led by Jonathan Sebat, PhD, assistant professor of psychiatry and cellular and molecular medicine at the University of California, San Diego School of Medicine, has identified a gene mutation strongly linked to the brain disorder – and a signaling pathway that may be treatable with existing compounds.

The work poses significant and immediate implications for neurobiology and the treatment of schizophrenia because the gene identified by the researchers is an especially attractive target for drug development.

“In some ways, this is the kind of gene that the pharmaceutical industry has been waiting for,” said Sebat, who is also chief of the Beyster Center for Molecular Genomics of Neuropsychiatric Diseases and a member of the Institute for Genomic Medicine, both at UC San Diego. “Its activity can be modulated by synthetic peptides; and some have already been created.”

The findings are published in the Feb. 3, 2011 online issue of the journal Nature.
Schizophrenia is a chronic, severe and disabling brain disorder, with symptoms that include hallucinations, delusions and thought disorders. It is believed to be caused by environmental and genetic factors, most notably the latter: the illness occurs in 1 percent of the general population, or 10 percent of people who have a first-degree relative with the disorder, such as a parent or sibling.

In previous work, Sebat and collaborator Mary-Claire King, a professor of medical genetics at the University of Washington, discovered that rare mutations at many locations in the human genome resulted in significantly higher risk of schizophrenia. These mutations consisted of copy number variants or CNVs – a type of genetic variation in which the number of copies of a gene differs between individuals. The findings were the first conclusive evidence that rare mutations can cause schizophrenia, but they did not identify the specific genes involved.

The latest study goes much further. Researchers scanned for CNVs in the genomes of 8,290 individuals with diagnosed cases of schizophrenia and 7,431 healthy controls. “We found very strong links to multiple sites in the genome,” said Sebat. “Some had been picked up before in earlier studies, but we uncovered a very important new finding: duplications at the tip of chromosome 7q were detected in individuals with schizophrenia at a rate14 times higher than in healthy individuals. These CNVs impact a gene that is important for brain development – the neuropeptide receptor VIPR2.”

Formally known as the Vasoactive Intestinal Peptide Receptor 2, VIPR2 is expressed in the nervous system, including in the brain, blood vessels and gastrointestinal tract. Previous studies have shown that VIPR2 helps to regulate the formation and activity of neurons in the brain. In mice, VIPR2 also has been found to play important roles in behavioral processes, including learning and timing of daily activity.

Read in Full: http://www.medicalnewstoday.com/articles/215535.php

Van Gogh

By Bill George, MA Cantab

I was very nervous when my editorial about schizophrenia — there we go, a word I ought not to be using — appeared Open Access online in the December 2010 Journal of Mental Health (published by Informa Healthcare, New York). It contains personal details which it is not customary to reveal. Having got over that I had more anxiety when the printed journal was delayed by a month for unknown reasons. Now that it’s out I am calm again.

Why should I not be using the ‘S’ word? What’s in a name?

The answer is that it has acquired a stigma in the course of a hundred years owing to the small minority of people with our condition who are violent and attack or kill other people.

Furthermore, according to Jim van Os, a professor of psychiatry at Maastricht University in the Netherlands and an invited member of the American Psychiatric Association’s DSM 5 Psychotic Disorders Work Group, the diagnosis may itself be a source of stigma. It is mystifying and confusing: people with schizophrenia do not have a split personality; the condition does not, according to Jim, exist as a distinct illness; it is a ragbag of symptoms such that calling it anything other than a syndrome is totally misleading.

So what name are the Work Group going to recommend to the APA? Probably “psychotic syndrome.” Now we, as consumers — for I am one — do not find that appealing. It is pathological. “I am a psycho” sounds weird.

What are the alternatives? It could be called “the Bleuler syndrome” after the Swiss professor of psychiatry who put forward the word schizophrenia in 1908 to replace the previously stigmatized term dementia praecox, or premature senility.

Another suggestion is made by Anoiksis, the Dutch consumer association of which I am a member: Dysfunctional Perception Syndrome (DPS). But I find the dysfunctional bit negative and tend to shorten it to Perception Syndrome. After all the medical term syndrome already implies an illness or disorder of some kind.

Also, to me, and here I am being disloyal to my own Anoiksis club, the word perception suggests sense data – seeing, hearing, tasting, smelling, feeling, … and does not capture the characteristic of a hallucination, let alone a delusion or any of the other, sometimes negative, symptoms.

Read in Full: http://psychcentral.com/blog/archives/2011/02/02/does-schizophrenia-need-a-new-name/

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