Excellent article on the genetics and biochemistry of schizophrenia which may lead to new treatment
The Swedish scientist Arvid Carlsson had discovered dopamine in the early 1950s, and a decade later he and his colleagues determined that antipsychotic drugs worked by blocking dopamine from attaching to its receptor molecules. This finding dovetailed with another serendipitous finding: as early as the 1930s, it had been noted that amphetamine could cause psychosis. Amphetamine and other psychostimulants, it turns out, boost the activity of dopamine. Thus, the “dopamine hypothesis” of schizophrenia was born.
For the next several decades, researchers focused on trying to understand how dopamine systems were disturbed in the disorder. However, despite some significant refinements to chlorpromazine, especially reductions of some side effects, this line of research has been disappointing. According to Joseph Coyle of Harvard University, one of the first schizophrenia researchers to turn their attention to glutamate, 70 to 80 percent of patients with schizophrenia treated with dopamine drugs remain profoundly impaired by cognitive and negative symptoms. Moreover, neither a clear understanding of how blocking dopamine receptors curbs psychosis nor any new molecular targets have emerged from this line of research. Most psychiatry researchers are currently of the opinion that the dysfunction of dopamine neurotransmission in schizophrenia results from, or compensates for, a more fundamental or “upstream” disturbance of the nervous system, perhaps in glutamate signaling.
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