Impact of Vitamin B12, Folate and Homocysteine in Modulating Cognitive Functions and the Brain’s White Matter Hyperintensity in Alzheimer’s Disease

Background Deficiency of vitamin B12 and folate as surrogate factors attributed to cognitive deterioration among older adults with Alzheimer’s disease (AD). Increased homocysteine levels >15 µmol/L (hyperhomocysteinaemia) due to insufficiency of vitamin B12 contribute to damage to the small blood vessels in the brain and aggravate the white matter lesion. Purpose The study aimed to determine the impact of B12, folic acid and homocysteine in modulating cognitive functions and white matter hyperintensity in AD. Methods A case-control study of a total number of 82 patients (41 AD patients and 41 controls) was recruited. The cognitive functions were assessed by the Montreal Cognitive Assessment (MoCA), and white matter hyperintensity was marked by magnetic resonance imaging studies. The levels of vitamin B12, folic acid and homocysteine in serum were also assessed. Results The noticeable changes were observed in the cognitive scores and levels of B12, folic acid and homocysteine in AD and controls and found statistically significant ( p < .001). Spearman’s rank correlations revealed that cognitive functions (MoCA score) showed a direct correlation with B12 ( ρ = 0.513, p < .001). Conversely, MoCA was moderately negatively correlated with homocysteine ( ρ = −0.422, p < .001). Participants with B12 deficiency showed a significantly higher frequency of white-matter hyperintensities (WMH) ( χ ² = 4.654, p = .031; Fisher’s exact p = .048). Conclusion Nutrient deficiencies, especially B12, have a disruptive impact on cognitive domains and WMH in AD, which could be considered as key indicators to identify the disease severity among older adults. Recommendations of vitamin B12 plus supplements might be connected to clinical and public health initiatives to halt the rate of progression of cognitive decline in AD.