Originally published November 1 2005
Stanford researchers find genetic condition that contributes to schizophrenia
by Mike Adams, the Health Ranger, NaturalNews Editor
Researchers at the Stanford University School of Medicine, Lucile Packard Children's Hospital and the University of Geneva have found that a gene that controls dopamine levels is linked to schizophrenia.
Reiss is the Robbins Professor of Psychiatry and Behavioral Sciences at Stanford and director of the school's Center for Interdisciplinary Brain Sciences Research.
Data from this and other studies suggest a kind of Goldilocks effect for this important chemical messenger: too little or too much can dramatically interfere with normal cognition, behavior and motor skills.
Schizophrenia is a brain disease that affects about 1 percent of people in this country and can manifest itself through agitation, catatonia and psychosis.
Scientists have suspected for many years that dopamine was involved, due in part to the success of older psychiatric drugs that function by interacting with dopamine receptors in the brain.
Reiss and the study's first author Doron Gothelf, MD, a child psychiatrist and postdoctoral scholar at Stanford, studied 24 children with a small deletion in one copy of chromosome 22.
About 30 percent of children with this deletion, which occurs in about one in 4,000 births, will develop schizophrenia or a related psychotic disorder.
Because most people have two copies of the gene, it doesn't usually matter which versions of COMT they inherit; high-high, high-low and low-low all seem to provide enough COMT activity to get the job done (though some combinations confer a mild advantage for some cognitive tasks).
Reiss and Gothelf, who is also an assistant professor at Tel Aviv University in Israel, surmised that a single copy of the low-activity COMT might not dispose of enough dopamine to produce optimal brain function.
"What's interesting about this finding is that the disease course in the individuals with low-activity COMT looked remarkably like idiopathic schizophrenia," said Reiss, who hopes to use this and future data to develop a model for other causes of schizophrenia.
"Although this deletion probably causes less than 5 percent of schizophrenia cases, it's the only well-defined genetic risk factor we have right now," said Reiss.
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