Abstract
It has been suggested that the BDNF Val66Met polymorphism modulates episodic memory performance via effects on hippocampal neural circuitry. However, fMRI studies have yielded inconsistent results in this respect. Moreover, very few studies have examined the effect of met allele load on activation of memory circuitry. In the present study, we carried out a comprehensive analysis of the effects of the BDNF polymorphism on brain responses during episodic memory encoding and retrieval, including an investigation of the effect of met allele load on memory related activation in the medial temporal lobe. In contrast to previous studies, we found no evidence for an effect of BDNF genotype or met load during episodic memory encoding. Met allele carriers showed increased activation during successful retrieval in right hippocampus but this was contrast-specific and unaffected by met allele load. These results suggest that the BDNF Val66Met polymorphism does not, as previously claimed, exert an observable effect on neural systems underlying encoding of new information into episodic memory but may exert a subtle effect on the efficiency with which such information can be retrieved.
Highlights
Brain-Derived Neurotrophic Factor (BDNF) is a secretory protein that is widely distributed in the human brain with its expression reduced in neurodegenerative disorders including Alzheimer’s and Huntington’s disease [1]–[5]
Repeated measures Analysis of Variance (ANOVA) comparing successful encoding activation in met carriers (MetMet and ValMet) and val homozygotes in the medial temporal lobe (MTL) ROIs revealed no main effect of group, F(1,57) = .32, p = .57 and no group x ROI interaction, F(1,57) = 1.16, p =
Voxelwise searches across bilateral hippocampus and parahippocampal gyrus, and across regions activated in the whole-brain task analysis, with a family-wise error rate (FWE)-corrected p-value of 0.05, revealed no voxels that showed a significant effect of group on activation during successful encoding, comparing val homozygotes with either met homozygotes or with met carriers
Summary
Brain-Derived Neurotrophic Factor (BDNF) is a secretory protein that is widely distributed in the human brain with its expression reduced in neurodegenerative disorders including Alzheimer’s and Huntington’s disease [1]–[5]. [11] [20]; [14] [19], with alpha levels ranging from 0.05 to 0.001 and extent thresholds (minimum cluster size for significance) ranging from 0 to 10 voxels The majority of these studies have reduced the number of comparisons carried out by restricting their analyses to regions in the MTL. Even with an alpha level of 0.001, without a correction for multiple comparisons we would expect to see significant effects in several voxels merely by chance With such a range of statistical approaches, it is perhaps unsurprising that different studies have observed widely different results. Of the very few studies that have examined the effects of genotype on activation during successful memory encoding and retrieval, results are inconsistent, with some showing no genotype effect [19] and some showing a difference between genotype groups but only with an uncorrected statistical threshold [20]. For comparability with previous studies, we examined effects of genotype on a scene encoding and recognition memory task that was adapted from one used in a previous study on the effects of the BDNF Val66Met polymorphism on memory related brain activation [17]
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