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Reading deficits in schizophrenia and individuals at high clinical risk: relationship to sensory function, course of illness, and psychosocial outcome.

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Lower expression of glutamic acid decarboxylase 67 in the prefrontal cortex in schizophrenia: contribution of altered regulation by Zif268.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kimoto, Sohei Bazmi, H. Holly Lewis, David A.
Abstract	OBJECTIVE: Cognitive deficits of schizophrenia may be due at least in part to lower expression of the 67-kDa isoform of glutamic acid decarboxylase (GAD67), a key enzyme for GABA synthesis, in the dorsolateral prefrontal cortex of individuals with schizophrenia. However, little is known about the molecular regulation of lower cortical GAD67 levels in schizophrenia. The GAD67 promoter region contains a conserved Zif268 binding site, and Zif268 activation is accompanied by increased GAD67 expression. Thus, altered expression of the immediate early gene Zif268 may contribute to lower levels of GAD67 mRNA in the dorsolateral prefrontal cortex in schizophrenia. METHOD: The authors used polymerase chain reaction to quantify GAD67 and Zif268 mRNA levels in dorsolateral prefrontal cortex area 9 from 62 matched pairs of schizophrenia and healthy comparison subjects, and in situ hybridization to assess Zif268 expression at laminar and cellular levels of resolution. The effects of potentially confounding variables were assessed in human subjects, and the effects of antipsychotic treatments were tested in antipsychotic-exposed monkeys. The specificity of the Zif268 findings was assessed by quantifying mRNA levels for other immediate early genes. RESULTS: GAD67 and Zif268 mRNA levels were significantly lower and were positively correlated in the schizophrenia subjects. Both Zif268 mRNA-positive neuron density and Zif268 mRNA levels per neuron were significantly lower in the schizophrenia subjects. These findings were robust to the effects of the confounding variables examined and differed from other immediate early genes. CONCLUSIONS: Deficient Zif268 mRNA expression may contribute to lower cortical GAD67 levels in schizophrenia, suggesting a potential mechanistic basis for altered cortical GABA synthesis and impaired cognition in schizophrenia.
File Format	HTM / HTML
ISSN	0002953X
e-ISSN	15357228
DOI	10.1176/appi.ajp.2014.14010004
Journal	American Journal of Psychiatry
Issue Number	9
Volume Number	171
Language	English
Publisher	American Psychiatric Association
Publisher Date	2014-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Psychiatry Antipsychotic Agents Pharmacology Cognition Disorders Glutamate Decarboxylase Prefrontal Cortex Schizophrenia Gamma-aminobutyric Acid Biosynthesis Animals Autopsy Etiology Genetics Confounding Factors (epidemiology) Disease Models, Animal Drug Monitoring Gene Expression Regulation, Enzymologic Chemistry Isoenzymes Macaca Fascicularis Metabolism Pathology Promoter Regions, Genetic Complications Drug Therapy Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Psychiatry and Mental Health

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