TY - JOUR
TI - Excess of allele1 for alpha 3 subunit GABA receptor gene (GABRA3) in
bipolar patients: a multicentric association study
AU - Massat, I
AU - Souery, D
AU - Del-Favero, J
AU - Oruc, L
AU - Noethen, MM
AU - and Blackwood, D
AU - Thomson, M
AU - Muir, W
AU - Papadimitriou, GN and
AU - Dikeos, DG
AU - Kaneva, R
AU - Serretti, A
AU - Lilli, R
AU - Smeraldi, E
AU - and Jakovljevic, M
AU - Folnegovic, V
AU - Rietschel, M
AU - Milanov, V and
AU - Valente, F
AU - Van Broeckhoven, C
AU - Mendlewicz, J
JO - Journal of Molecular Psychiatry
PY - 2002
VL - 7
TODO - 2
SP - 201-207
PB - Nature Publishing Group
SN - 2049-9256
TODO - 10.1038/sj.mp.4000953
TODO - GABRA3; association study; candidate gene; chromosome X; bipolar
disorder
TODO - 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.
ER -