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Neurodevelopmental Model of Schizophrenia

Richard Lewine, PhD
Arch Gen Psychiatry. 1988;45(11):1051-1052. doi:10.1001/archpsyc.1988.01800350085014.
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—Weinberger has presented a series of thought-provoking articles the primary thesis of which is that a latent "lesion" in the dorsolateral prefrontal cortex, revealed only at sexual maturation, interacts with the appropriate genetic predisposition to result in the clinical manifestation of schizophrenia.1,2 Such an interaction could account not only for the particular cognitive and affective dysfunctions of schizophrenia but also for the well-documented tendency of schizophrenia to present floridly in adolescence, the period of full sexual maturation. Elsewhere, Weinberger has pointed to evidence of a later peak and slower regression of dopamine activity among women to account for a later age of onset and less malignant course of the disorder in women. Underlying the entire model is a 1980s version of the "dopamine hypothesis"; mesolimbic overactivity and mesocortical underactivity account for positive and negative symptoms, respectively.

Weinberger's argument assumes a "triggering" concept of etiology, that is, the "coming

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