Unformatted text preview: rch indicates that the strong genetic influence on the risk of developing a disorder such as schizophrenia is not the work of a single gene. Rather, the increase in risk seems to be an aggregate effect of many genes interacting with one another and with nongenetic factors. By studying the DNA sequences of people with schizophreFrom an early age, STEVEN E. HYMAN was curious about how our brains underlie thinking, emotion and behavioral control. He studied philosophy as an undergraduate at Yale University and philosophy of science at the University of Cambridge, where he was a Mellon Fellow. After earning his M.D. at Harvard University, he received clinical training in psychiatry and scientific training in molecular neurobiology. He was the founding director of Harvard's Interfaculty Initiative in Mind, Brain and Behavior. From 1996 to 2001 he served as Director of the National Institute of Mental Health, the component of the National Institutes of Health charged with generating the knowledge needed to understand, treat and prevent mental illness. Since 2001 he has been Harvard's provost and a professor of neurobiology at Harvard Medical School.
SCIENTIFIC AMERICAN THE AUTHOR www.sciam.com 99 COPYRIGHT 2003 SCIENTIFIC AMERICAN, INC. nia and their family members, researchers have already found several genetic variations that appear to increase susceptibility to the disorder [see illustration on preceding page]. These variations occur in genes that code proteins involved in the transmission of signals among neurons in the brain, so it is possible that the variations disrupt that process. Similar studies have identified genetic variations that appear to increase the risk of developing major depression and bipolar disorder. Furthermore, a variation of HOXA1, a gene related to early brain development, seems to boost susceptibility to autism. The variant gene is present in about 20 percent of the general population but in about 40 percent of people with autism. Although possessing the variation of HOXA1 approximately doubles the risk of developing autism, more than 99.5 percent of people who have the variant gene do not acquire the disorder, and about 60 percent of people with autism do not possess the variant gene. As is the case for many diseases, there is not likely to be a single set of genes arrays of thousands of reference DNA samples-- researchers can also discover which genes are actively coding proteins in a given cell or tissue. If the gene-hunting effort is successful, doctors will someday be able to analyze a patient's genetic sequence and see where it fits in the matrix of risks. The accuracy of this matrix would be greatly enhanced if physicians also had more information about environmental risk factors. In all likelihood, none of th...
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This note was uploaded on 05/02/2010 for the course PSY 320 taught by Professor Na during the Spring '10 term at Suffolk.
- Spring '10