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NEW YORK (Reuters Health) Jan 16 - A diet that contains inadequate amounts of the B vitamin folate may raise the risk of Parkinsonīs disease, new research in mice suggests.
The study found that dopamine-producing cells in the brain were more susceptible to damage and death when mice consumed a folate-deficient diet. Folate-deficient mice also had elevated levels of homocysteine, the report indicates. In addition, high concentrations of homocysteine infused directly into the brain exacerbated the Parkinsonīs-like symptoms in the mice.
While previous studies have shown that levels of homocysteine are elevated in people with Parkinsonīs disease, the precise role of homocysteine in the development of the disease has remained unclear, lead author Dr. Mark P. Mattson told Reuters Health.
"Our findings...strongly suggest that elevated homocysteine levels can indeed render neurons vulnerable to Parkinsonīs disease," said Dr. Mattson, a scientist with the National Institutes on Aging Gerontology Research Center, a division of the National Institutes of Health in Baltimore, Maryland.
He recommends that patients and individuals with a family history of Parkinsonīs disease take a daily supplement containing 400 micrograms of folic acid, a vitamin that has been shown to reduce homocysteine levels and now appears to allow nerve cells to repair their damaged DNA and continue to function properly.
In the study, published in the January issue of the Journal of Neurochemistry, researchers fed a group of mice a diet containing adequate levels of folate and another group of mice a folate-deficient diet. After 3 months they injected mice with MPTP, a chemical that induces Parkinsonīs-like symptoms.
Mice fed a folate-deficient diet showed more severe symptoms and had blood homocysteine levels eight times higher than mice fed a diet with folate.
"Our findings establish that a diet with low folic acid levels increases homocysteine levels and the homocysteine, in turn, renders neurons in the brain vulnerable to dysfunction and death," Dr. Mattson concluded.
J Neurochem 2002;80:101-110.
From:
http://neurology.medscape.com/reuters/prof/2002/01/01.17/20020116scie002.html
Reprinted from:
Look here: 20020116scie002.html