BDNF (rs6265) Val < Met polymorphism can buffer cognitive functions against post stroke CT/MRI pathological findings.

Brain lesions following stroke have been shown prevalently in CT/MRI, and it was confirmed that lesions usually are accompanied by cognitive deficits. Although previous studies have emphasized that BDNF Val66Met polymorphism had a substantial role in neurogenesis and synaptic plasticity, it remains unclear to what extent an interaction may be appeared between neuroimaging findings and Val66Met variants on different cognitive functions following stroke. In a case-control study the carriers of at least one Val allele (n = 56), were compared with the carriers of Met/Met homozygotes (n = 156) in order to find possible neuroimaging factors in relation to cognitive functions in a sample from the north of Iran. The third edition of Addenbrooke's Cognitive Examination (ACE-III) was used to determine the cognitive functions. There were interactive effects among Val66Met genotypes with dominant hemisphere lesions [F = 6.97, ή2 = 0.03, p = 0.009], cerebral atrophy [F = 5.43, ή2 = 0.03, p = 0.011] and number of lesions [F = 4.32, ή2 = 0.04, p = 0.014], for visuospatial skills, memory, and attention functions respectively; implying that the effect of dominant hemisphere lesions, cerebral atrophy, and multiple lesions on cognitive functions have been modulated by Met/Met homozygosity. The destructive effect of Val/Met homozygosity on cognitive functions was shown to be exacerbated by dominant hemispheric lesions, cerebral atrophy, and multiple lesions following stroke. The findings of present research support our hypothesis that interaction of Val66Met variants with cerebral lesions is associated with cognitive dysfunctions in post stroke conditions; particularly through Met/Met homozygosity which act as a buffer mechanism against some CT/MRI pathological findings.