Vitamin B Supplementation Did Not Slow Cognitive Decline In Patients With Alzheimer's Disease
October 24, 2008
Adapted from the JAMA and Archives Journals
High-dose vitamin B supplementation for patients with mild to moderate Alzheimer disease did not slow the rate of cognitive decline, according to a study in the October 15, 2008 issue of the Journal of the American Medical Association (JAMA).
Evidence of homocysteine (an amino acid produced by the body) elevation in Alzheimer disease (AD) and the involvement of homocysteine in neuropathological mechanisms suggest that reduction of homocysteine may offer an approach to altering the disease. B vitamins that influence homocysteine metabolism have been considered as a therapeutic option to reduce risk of AD or slow its progression, according to background information in the article. According to the authors, prior studies of B vitamins to reduce homocysteine in AD have not had sufficient size or duration to assess their effect on cognitive decline.
Paul S. Aisen, M.D., of the University of California, San Diego, and colleagues conducted a clinical trial to determine if reduction of homocysteine levels with high-dose supplementation with folic acid and vitamins B6 and B12 for 18 months would slow the rate of cognitive decline in 409 individuals with mild to moderate AD.
The researchers found that even though the vitamin supplement regimen was effective in reducing homocysteine levels, it had no beneficial effect on primary cognitive functions.
"Many studies suggest that relative elevation of homocysteine is characteristic of AD, and laboratory research implicates homocysteine in neurodegenerative mechanisms. High-dose B vitamin supplementation in individuals with normal levels of B vitamins was effective in reducing homocysteine levels. However, our study does not support the treatment of individuals with mild to moderate AD and normal vitamin levels with B vitamin supplements," the authors conclude.
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