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Retinoid Dysregulation May Result in Abnormal Expression of Glutamic Acid Decarboxylase in Schizophrenia

Ann B. Goodman; Nathan S. Kline
Arch Gen Psychiatry. 1996;53(7):653. doi:10.1001/archpsyc.1996.01830070103015.
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Akbarian et et al1 argue convincingly for abnormal expression of the enzyme glutamic acid decarboxylase (GAD) in the prefrontal cortex of a small sample of schizophrenic brains compared with controls. The authors suggest 4 mechanisms to account for this intriguing finding: (1) a genetic defect in the GAD protein, (2) a pathogenic agent, (3) a developmental defect in cell circuitry resulting in hypoactivity of the prefrontal cortex, and (4) a second-trimester environmental insult affecting the development of the cortical subplate. Except for mutation in the GAD gene, each of these mechanisms could be the result of abnormal function of the vitamin A (retinoid) cascade.

Review of the action and metabolism of genes of the retinoid cascade in relation to schizophrenia indicates that, in addition to controlling for neuronal migration and anterior and posterior positional development of the central nervous system, retinoids are present in all areas of the brain,


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