Excess of Allelel for Alpha3 Subunit GABA Receptor Gene (GABRA 3) in Bipolar Patients: A Multicentric Assocation Study (CROSBI ID 103776)
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Massat, I. ; Souery, D. ; Del-Favero, J. ; Oruč, L. ; Noethen, M.M. ; Blackwood, D. ; Thomson, M. ; Muir, W. ; Papadimitiou, G.N. ; Dikeos, D.G. ; Kaneva, R. ; Serrretti, A. ; Lilli, R. ; Smeraldi, E. ; Jakovljević, M. ; Folnegović-Šmalc, Vera ; Rietschel, M. ; Milanova, V. ; Valente, F. ; Van Broeckhoven, C. ; Mendlewitz, J.
engleski
Excess of Allelel for Alpha3 Subunit GABA Receptor Gene (GABRA 3) in Bipolar Patients: A Multicentric Assocation Study
The available data from preclinical and pharmacological studies on the role of gamma amino butyric acid (GABA) support the hypothesis that a dysfunction in brain GABAergic system activity contributes to the vulnerability to bipolar affective disorders (BPAD). Moreover, the localization of the alpha3 subunit GABA receptor GABRA3 gene on the Xq28, a region of interest in certain forms of bipolar illness, suggests that GABRA3 may be a candidate gene in BPAD. In the present study, we tested the genetic contribution of the GABRA3 dinucleotide polymorphism in a European multicentric case-control sample, matched for sex and ethnogeographical origin. Allele and genotype (in females) frequencies were compared in 185 BPAD patients and 370 controls. A significant increase of genotype 1-1 was observed in BPAD females compared to controls (P=0.0004). Furthermore, when considering recessivity of allele 1 (females with genotype 1-1 and males carrying allele 1), results were even more significant (P= 0.00002). Our findings suggest that the GABRA3 polymorphism may confer susceptibility to or may be in linkage disequilibrium with another gene involved in the genetic etiology of BPAD.
GABA; GABRA3; BPAD
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