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

Area of Science:

• Neuroscience
• Genetics
• Radiology

Background:

• Stroke-induced brain lesions are frequently linked to cognitive impairments.
• The BDNF Val66Met polymorphism influences neurogenesis and synaptic plasticity, but its interaction with neuroimaging findings in post-stroke cognition is not fully understood.

Purpose of the Study:

• To investigate the interaction between BDNF Val66Met genotypes and neuroimaging findings (lesion location, cerebral atrophy, lesion count) on cognitive functions in stroke survivors.

Main Methods:

• A case-control study compared BDNF Val66Met genotypes (Val allele carriers vs. Met/Met homozygotes) in a North Iranian sample.
• Cognitive functions were assessed using the Addenbrooke's Cognitive Examination (ACE-III).
• Statistical analyses examined interactive effects between genotypes and neuroimaging data.

Main Results:

• Significant interactions were found between Val66Met genotypes and dominant hemisphere lesions, cerebral atrophy, and lesion count, affecting visuospatial skills, memory, and attention.
• Met/Met homozygosity appeared to modulate the impact of these neuroimaging factors on cognitive performance.
• Val/Met heterozygosity exacerbated cognitive deficits when combined with dominant hemispheric lesions, cerebral atrophy, or multiple lesions.

Conclusions:

• The interaction between BDNF Val66Met variants and cerebral lesions significantly influences cognitive outcomes post-stroke.
• Met/Met homozygosity may offer a protective effect against cognitive decline by buffering the impact of certain neuroimaging pathologies.