THE POTENTIAL FOR
NEUROPROTECTION THROUGH FOLATE SUPPLEMENTATION AND HOMOCYSTEINE-LOWERING IN ALZHEIMER'S DISEASE
Aron Troen
Nutrition and Neurocognitive Laboratory, Jean Mayer USDA Human
Nutrition Research Centre on Aging at Tufts University, 711 Washington
Street, Boston MA 02111-1524
Alzheimer Disease (AD) is a devastating and debilitating
neurodegenerative condition, and the most common cause of dementia
among the elderly. Despite considerable advances in the cellular and
molecular pathology of AD, little progress has been made in
understanding the primary causes of the disease, and it remains
incurable. Strong epidemiological evidence for an association of AD,
stroke and other neurological disorders with low blood levels of folate
and elevated plasma total homocysteine (a risk factor for vascular
disease and stroke) is of considerable interest in this regard. These
associations implicate disrupted homocysteine metabolism as a factor in
age-related cognitive decline. Several theoretically plausible
mechanisms have been proposed to explain how low folate or high blood
homocysteine might promote neurodegeneration. However, these
mechanisms have yet to be adequately demonstrated in vivo and it
remains uncertain whether they are causally related to cognitive
decline. Nevertheless, plasma homocysteine can be safely lowered by
nutritional intervention using vitamin supplements, thus raising the
possibility of lowering the risk of dementia by specific vitamin
therapy. Several intervention trials are currently underway to
determine the efficacy of dietary folate supplements in combination
with other B-vitamins in slowing cognitive decline in Alzheimer's
disease and stroke.
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