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Folate, Homocysteine, and Neurological Function

Authors

  • Martha Savaria Morris PhD

    1. Nutritional Epidemiology Program, Jean Mayer USDA Human Nutrition Research Center
      on Aging at Tufts University, Boston, Massachusetts
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Reprint requests to Martha Savaria Morris, Nutritional Epidemiology Program, Jean Mayer USDA HNRC at Tufts University, 711 Washington Street, 9th Floor, Boston, MA 02111. E-mail: Morris@HNRC.Tufts.edu

Abstract

The study of different neurological problems, including stroke, Alzheimer's disease (AD), and depression, has propelled a greater interest in interrelationships among folate, homocysteine, and neurological function. Specifically, low folate status is a suspected risk factor for depression that also results in an increase in circulating levels of the sulfur amino acid homocysteine. Homocysteine has emerged as an independent risk factor for stroke, and recent studies suggest that vascular disease affecting the brain and Alzheimer's disease may result together in senile dementia. The relationship between stroke and AD was at first interpreted as coincidence, given the pathologic distinctions between the two diseases. However, the connection is now hypothesized to reflect some common pathogenic factors involving folate, homocysteine, or both. It remains unclear whether there is a causal relationship between neurological dysfunction in either condition with folate or homocysteine. Nevertheless, since improvement of folate status lowers homocysteine levels, the hypothesis that folate supplementation may lower the risk of several important health consequences of aging, including various forms of neuropsychiatric dysfunction, is worthy of current intensive exploration.

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