BDNF and TNF-α polymorphisms in memory

Abstract

Here, we investigate the genetic basis of human memory in healthy individuals and the potential role of two polymorphisms, previously implicated in memory function. We have explored aspects of retrospective and prospective memory including semantic, short term, working and long-term memory in conjunction with brain derived neurotrophic factor (BDNF) and tumor necrosis factor-alpha (TNF-α). The memory scores for healthy individuals in the population were obtained for each memory type and the population was genotyped via restriction fragment length polymorphism for the BDNF rs6265 (Val66Met) SNP and via pyrosequencing for the TNF-α rs113325588 SNP. Using univariate ANOVA, a significant association of the BDNF polymorphism with visual and spatial memory retention and a significant association of the TNF-α polymorphism was observed with spatial memory retention. In addition, a significant interactive effect between BDNF and TNF-α polymorphisms was observed in spatial memory retention. In practice visual memory involves spatial information and the two memory systems work together, however our data demonstrate that individuals with the Val/Val BDNF genotype have poorer visual memory but higher spatial memory retention, indicating a level of interaction between TNF-α and BDNF in spatial memory retention. This is the first study to use genetic analysis to determine the interaction between BDNF and TNF-α in relation to memory in normal adults and provides important information regarding the effect of genetic determinants and gene interactions on human memory.

The BDNF Val66Met Polymorphism Influences Reading Ability and Patterns of Neural Activation in Children

“…These findings are consistent with the previously documented association in adults between the Val 66 Met polymorphism in the BDNF gene and memory and cognitive function [15–21]. …”

“…BDNF protein is a neurotrophin that influences many neural events related to brain plasticity [14] by regulating cell survival, proliferation and synaptic growth, and by modulating synaptic changes, particularly long-term potentiation (LTP) in the hippocampus. Individuals homozygous for the ancestral G allele (i.e., Val/Val homozygotes), when compared to heterozygous individuals (i.e., Val/Met) or individuals homozygous for the derived A allele (i.e., Met/Met), generally perform better in a variety of domains of cognition, including memory [15–21] attention [22–26], and executive function [3, 8, 27, 28], although this pattern of results is not always consistent in studies of BDNF and cognition (see Mandelman and Grigorenko [11] for a review).…”

Interaction of BDNF with cytokines in chronic schizophrenia

“…This association is consistent with the results by Yogeetha et al (2013), who reported a significant interactive effect on spatial memory retention in healthy individuals by the polymorphisms BDNF rs6265 (Val66-Met), which lowers BDNF levels, and TNF-a rs113325588, which lowers TNF-a levels. Although these associations do not offer a causal pathophysiology, it has been shown that the disrupted TNF-a signaling impairs the development of the hippocampus and causes cognitive dysfunction (Garay and McAllister, 2010;Baune et al, 2012).…”

BDNF Variants May Modulate Long-Term Visual Memory Performance in a Healthy Cohort

“…Our results demonstrated significant effects of BDNF on long-term visual memory ( p -value = 0.003), and we found that the Val/Val genotype was linked with poorer visual memory [28]. In the present work, we extended our investigation of variants involved in visual memory performance to 38 SNPs in both the BDNF and BDNF-AS genes in a larger cohort of healthy individuals ( n = 597).…”