Περίληψη:
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.
Συγγραφείς:
Massat, I
Souery, D
Del-Favero, J
Oruc, L
Noethen, MM
and Blackwood, D
Thomson, M
Muir, W
Papadimitriou, GN and
Dikeos, DG
Kaneva, R
Serretti, A
Lilli, R
Smeraldi, E
and Jakovljevic, M
Folnegovic, V
Rietschel, M
Milanov, V and
Valente, F
Van Broeckhoven, C
Mendlewicz, J
