Pharmacologic implications of neurobiological models of schizophrenia.
The dopamine model of schizophrenia has been supplanted by several additional models in order to account for genetic findings, risk factors, course of illness, and the diversity of symptom domains. The increasing number and complexity of potential models for this heterogeneous disorder offer new targets for pharmacologic treatment that differ in their appropriate time points for intervention and in their potential effects on the course of illness. This article reviews relevant neurodevelopmental, biochemical, and neurodegenerative models with respect to potential pharmacologic opportunities.
Goff
Donald C
DC
Department of Psychiatry, Harvard Medical School, Freedom Trail Clinic, 25 Staniford Street, Boston, MA 02114, USA. goff@psych.mgh.harvard.edu
D000975:Antioxidants / Q000627:therapeutic use*; D014150:Antipsychotic Agents / Q000494:pharmacology* / Q000627:therapeutic use*; D001921:Brain / Q000378:metabolism*; D004298:Dopamine / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors; D012559:Schizophrenia / Q000188:drug therapy / Q000453:epidemiology / Q000235:genetics
D000975:Antioxidants; D014150:Antipsychotic Agents; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid; D004298:Dopamine