A reporter once allegedly asked the infamous bank robber, Willie Sutton, why he robbed banks. Sutton's response was "Because that's where the money is" (1). Usingpostmortem humanbrain to elucidate the molecular biology of brain disease is a strategy consistent with Sutton's Law. The work of Ehringer and Hornykiewicz, which found decreased dopamine in the striatum of postmortem brains of patients with Parkinson's disease (2), was a resounding demonstration of the wisdom of this strategy. It paved the way for the use of L-dopa, the metabolic precursor of dopamine, in the treatment of Parkinson's disease (3). As dramatic as these findings were for neurology, it had a significant impact on the early postmortem brain studies of schizophrenia, which focused heavily on monoamines and their receptors (4-6). While the dramatic success of this approach for Parkinson's disease has not been matched as yet in psychiatric disorders, postmortem brain studies of schizophrenia have pushed ahead with a number of novel hypotheses propelled by advances from the Human Genome Project (7, 8) and the Psychiatric Ge-nomics Consortium (9). While studies related to risk variants for schizophrenia have involved hundreds of postmortem brains (10, 11), smaller, cellular-level studies have complemented this approach, as referenced in an article by Dienel et al. in this issue (12) entitled "The Nature of Prefrontal Cortical GABA Neuron Alterations in Schizophrenia: Markedly Lower Somatostatin and Parvalbumin Gene Expression Without Missing Neurons."
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