WEDNESDAY September 3, 2008 (foodconsumer.org) -- A new study in the August 26, 2008 issue of Proceedings of the National Academy of Sciences (PNAS) suggests that B-vitamin deficiency may cause vascular cognitive impairment.

The study was conducted in mice by researchers at Tufts University to examine the metabolic, cognitive, and microvascular effects of dietary B-vitamin deficiency.

"Metabolic impairments induced by a diet deficient in three B-vitamins -folate, B12 and B6- caused cognitive dysfunction and reductions in brain capillary length and density in our mouse model," says Aron Troen, PhD, the study's lead author. "The vascular changes occurred in the absence of neurotoxic or degenerative changes."

The study showed that mice on a diet deficient in folate, vitamin B12 and B6 experienced significant deficits in spatial learning and memory compared to those on a normal diet.

The study also showed that B-vitamin deficient mice had 7 times higher concentrations of homocysteine than those fed the normal diet. B-vitamins like folate vitamin B12 and vitamin B6 are needed to convert homocysteine back to methionine, a way to reduce accumulation of homocysteine.

High hommocysteine in the blood has been linked to increased risk of cognitive impairment although it is not clear whether this compound directly affects the risk.

In the current study, Troen and colleagues fed three diets to three groups of mice for 10 weeks and measured -vitamins and homocysteine and also assessed the brain anatomy and vasculature - arrangement of blood vessels in the brain.   Additionally, they also assessed cognitive functions.

"It took longer, on average, for the B-vitamin-deficient mice to maneuver the water maze, compared with controls," said Troen. "Longer latencies were associated with higher plasma homocysteine levels and shorter capillaries, particularly in the brain region called the hippocampus."

Troen added "Despite the vascular changes, the brain anatomy appeared normal, and there was no evidence of a cellular proliferation process called gliosis, which typically accompanies neurodegeneration."

Irwin Rosenberg, MD, director of the Nutrition and Neurocognition Laboratory at the HNRCA of Tufts noted "The elevated levels of homocysteine that were associated with vascular cognitive impairment in the mice in our study are comparable to the levels that are associated in older adults with an increased risk for Alzheimer's disease and cerebrovascular disease, the latter of which manifests with conditions such as stroke and atherosclerosis."

"These findings may indicate that microvascular changes mediate the association between high homocysteine levels and human age-related cognitive decline."