Association of Promoter Variants in the α7 Nicotinic Acetylcholine Receptor Subunit Gene With an Inhibitory Deficit Found in Schizophrenia

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Abstract
SCHIZOPHRENIA IS a complex disorder, in which heterogeneity, reduced penetrance, and environmental factors have made identification of genetic defects difficult. The work of many investigators has resulted in the discovery and replication of 8 principal linkage regions in the human genome. These include linkages at 1q21-q22,1 chromosome 6p22-p24,2 chromosome 6q21-q22,3 chromosome8p21-p22,4 chromosome 10p11-p15,5 chromosome13q14-q32,4 chromosome 15q13-q15,6-13 and chromosome 22q11-q13.14 Additional linkages on 6 other chromosomes may be contributory in some populations.15 In general, linkage in any given cohort is found in only a subset of the total number of families examined, suggesting that abnormalities in different gene sets may result in the same illness. Identification of pathogenic mutations in candidate genes that lie in the major linkage regions is necessary for a rigorous understanding of how several genes interact in the development of schizophrenia. Herein we present evidence that putative functional polymorphisms in the promoter region of the α7 neuronal nicotinic acetylcholine receptor subunit gene (CHRNA7 or α7), a candidate gene in the 15q13-q14 linkage region, are more frequently found in schizophrenia and are associated with a sensory deficit found in this common mental illness.

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