The BDNF Val66Met polymorphism affects amygdala activity in response to emotional stimuli: evidence from a genetic imaging study.

Mounting evidence shows that the brain derived neurotrophic factor (BDNF) plays a crucial role in synaptic plasticity. Due to its potential involvement in psychiatric diseases like depression and anxiety disorders BDNF lately became a major target in research. A functional variant of the BDNF gene--the BDNF Val66Met polymorphism--is of particular interest, because it influences the BDNF secretion which is followed by signaling at the TrkB receptor leading to dendritic growth of neurons. Findings from genetic association studies in humans yield heterogenous results with respect to the question of which allele represents a potential risk factor for an affective disorder. Although structural MRT studies revealed that the 66Met variant is associated with smaller hippocampi and could therefore present the risk allele, fMRI studies investigating the processing of emotion with respect to the BDNF Val66Met polymorphism are lacking. N=37 healthy female subjects participated in an fMRI experiment with an affective startle reflex paradigm. Carriers of the 66Met variant showed stronger amygdala activation in the right hemisphere in response to emotional stimuli compared to neutral stimuli. The results of this study add to growing literature, showing that it is the 66Met, which is associated with higher trait anxiety.