SAN FRANCISCO— Lower blood levels of vitamin B6 are inversely correlated with white matter lesions detected on MRI scans of patients clinically diagnosed with Alzheimer’s disease, investigators reported at the 56th Annual Meeting of the American Academy of Neurology. “This relation was independent from possible confounding factors such as cortical atrophy, hippocampal atrophy, and the MMSE [Mini-Mental State Examination],” said Frank-Erik de Leeuw, MD, PhD, of the Department of Neurology, University Medical Center St. Radboud, Nijmegen, the Netherlands.

VITAMINS AND VASCULAR DISEASE

Low levels of vitamin B6 due to poor dietary intake are not uncommon in the elderly and have been related to cognitive decline and memory dysfunction. However, the underlying mechanism is not known. Studies have suggested the effect of vitamin B6 on cognition may be mediated by vascular white matter lesions, given evidence that low vitamin B6 levels may result in premature vascular disease, possibly due to high levels of homocysteine. Previously, Dr. de Leeuw and colleagues found a linear relationship between white matter lesions and hippocampal atrophy in patients with probable Alzheimer’s disease, suggesting that vascular pathology and typical Alzheimer’s disease pathology are related.

Dr. de Leeuw said lower levels of vitamin B6 have been found among patients with Alzheimer’s disease but could not be correlated with vascular disease, possibly because the study sample included those with congestive heart failure and peripheral arterial disease. “We therefore set out to investigate the relation between the level of vitamin B6 and the presence of white matter lesions in patients with Alzheimer’s disease.”

Their study included 123 consecutive patients with probable Alzheimer’s disease for whom vitamin B6 and MRI scan data were available. Excluded were patients using food or vitamin supplements.

Plasma vitamin B6 status was measured by high performance liquid chromatography. White matter lesions were rated using a semiquantitative scale and were separately rated for the periventricular and subcortical regions. “We considered cortical atrophy, hippocampal atrophy, and the MMSE as a measurement of the severity of the duration of the disease, and we considered them as possible confounders,” Dr. de Leeuw said.

The mean age of the patients was 69.3, and 52% were women. The mean MMSE was 20.5; 28.5% of all participants had no white matter lesions and 40.8% had a medial temporal atrophy score ranging from 0 to 1. “Median hippocampal atrophy was about 1.5, the latter figure a relatively mildly demented population,” Dr. de Leeuw noted.

AN INVERSE RELATIONSHIP

Regression analysis showed a linear inverse relationship between vitamin B6 levels and degree of white matter lesions in the periventricular region. “Patients without white matter lesions had substantially higher levels of vitamin B6 compared to those with white matter lesions,” Dr. de Leeuw said.

“An identical observation was made for subcortical white matter lesions. At each standard deviation, increase of plasma level vitamin B6 was related to about halving the risk of ventricular white matter lesions and, for subcortical white matter lesions, an observation within the same magnitude was found, so high levels of vitamin B6 reduced risk of white matter lesions in both locations,” he added.

“It could be that vitamin B6 supplementation decreases the risk of these lesions and, consequently, the attendant cognitive decline,” Dr. de Leeuw concluded. “However, large prospective intervention studies are needed to unravel the chain of events from low vitamin B6 levels to dementia and a possible effect supplementation may have on cognition and a possible underlying mechanism.”

NR

—Debra Hughes

Suggested Reading
De Leeuw FE, Barkhof F, Scheltens P. White matter lesions and hippocampal atrophy in Alzheimer’s disease. Neurology. 2004;62:310-312.
Miller JW, Green R, Mungas DM, et al. Homocysteine, vitamin B6, and vascular disease in AD patients. Neurology. 2002;58:1471-1475.

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