BACKGROUND: Bcl-2 is a major regulator of neural plasticity and cellular resilience. A single nucleotide polymorphism (SNP) in the Bcl-2 gene, Bcl-2 rs956572, significantly modulates the expression of Bcl-2 protein and cellular vulnerability to apoptosis. We tested the hypothesis that this SNP would modulate gray matter (GM) volume in the limbic-cortical-striatal-pallidal-thalamic circuitry that plays major roles in mood regulation. METHODS: Forty-seven healthy subjects participated in this study (30 A carriers, 17 G homozygotes). Neuromorphometric differences between G homozygotes and A carriers were investigated using optimized voxel-based morphometry (VBM). Statistical significance was set at p < .05, corrected for multiple comparisons. RESULTS: A carriers showed less GM volume than G homozygotes in the left ventral striatum (p(corrected) < .05). CONCLUSIONS: Genetic variation in the Bcl-2 gene modulates GM volume in areas known to play key roles in the neurobiology of reward processes and emotion regulation and in the pathophysiology of mood disorders. Thus, the findings from the current study are noteworthy insofar as they converge with preclinical findings that Bcl-2 functions to enhance neuronal viability and might indirectly extend this evidence to humans.
BACKGROUND:Bcl-2 is a major regulator of neural plasticity and cellular resilience. A single nucleotide polymorphism (SNP) in the Bcl-2 gene, Bcl-2rs956572, significantly modulates the expression of Bcl-2 protein and cellular vulnerability to apoptosis. We tested the hypothesis that this SNP would modulate gray matter (GM) volume in the limbic-cortical-striatal-pallidal-thalamic circuitry that plays major roles in mood regulation. METHODS: Forty-seven healthy subjects participated in this study (30 A carriers, 17 G homozygotes). Neuromorphometric differences between G homozygotes and A carriers were investigated using optimized voxel-based morphometry (VBM). Statistical significance was set at p < .05, corrected for multiple comparisons. RESULTS: A carriers showed less GM volume than G homozygotes in the left ventral striatum (p(corrected) < .05). CONCLUSIONS: Genetic variation in the Bcl-2 gene modulates GM volume in areas known to play key roles in the neurobiology of reward processes and emotion regulation and in the pathophysiology of mood disorders. Thus, the findings from the current study are noteworthy insofar as they converge with preclinical findings that Bcl-2 functions to enhance neuronal viability and might indirectly extend this evidence to humans.
Authors: G J Moore; J M Bebchuk; K Hasanat; G Chen; N Seraji-Bozorgzad; I B Wilds; M W Faulk; S Koch; D A Glitz; L Jolkovsky; H K Manji Journal: Biol Psychiatry Date: 2000-07-01 Impact factor: 13.382
Authors: T Frodl; N Koutsouleris; R Bottlender; C Born; M Jäger; M Mörgenthaler; J Scheuerecker; P Zill; T Baghai; C Schüle; R Rupprecht; B Bondy; M Reiser; H-J Möller; E M Meisenzahl Journal: Mol Psychiatry Date: 2008-07-01 Impact factor: 15.992
Authors: Hilary P Blumberg; Fei Wang; Lara G Chepenik; Jessica H Kalmar; Elliot Kale Edmiston; Ronald S Duman; Joel Gelernter Journal: Biol Psychiatry Date: 2008-08-15 Impact factor: 13.382
Authors: Rodrigo Machado-Vieira; Natalia B Pivovarova; Ruslan I Stanika; Peixiong Yuan; Yun Wang; Rulun Zhou; Carlos A Zarate; Wayne C Drevets; Christine A Brantner; Amber Baum; Gonzalo Laje; Francis J McMahon; Guang Chen; Jing Du; Husseini K Manji; S Brian Andrews Journal: Biol Psychiatry Date: 2010-12-16 Impact factor: 13.382