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Dietary Folic Acid May Be Linked with Alzheimer's Risk

03/01/2002

BALTIMORE, Md.--Folic acid deficiency may be a factor in Alzheimer's disease risk, as well as elevated homocysteine levels, according to a study published in the March 1 issue of Journal of Neuroscience (22, 5:1752-62, 2002) (www.jneurosci.org). Scientists from the Laboratory of Neurosciences at the National Institute on Aging (NIA) (www.nia.nih.gov) noted this newly discovered link may help researchers discover the biochemical mechanisms for why people with high levels of homocysteine have nearly twice the risk of developing Alzheimer's. [For more on this topic, visit www.naturalproductsinsider.com/hotnews/22h14131852.html.]

"These new findings establish a possible cause-effect relationship between elevated homocysteine levels and degeneration of nerve cells involved in learning and memory in a mouse model of Alzheimer's disease," said Mark Mattson, Ph.D., chief of NIA's Laboratory of Neurosciences and a principal investigator on the NIA study.

NIA researchers studied two groups of transgenic mice, bred to develop Alzheimer's-like plaque in their brains. One group was fed a diet that contained normal amounts of folic acid, and the second group was fed a folate-deficient diet. In studying the mice's brains, researchers noted that the deficient group exhibited a decreased number of neurons in the hippocampus region. The hippocampus region of the brain was studied in particular because it is a critical center for learning and memory that is destroyed when Alzheimer's plaque accumulates, destroying neurons in the region.

An additional finding brought out during this animal study demonstrated that the folate-deficient group experienced a rise in homocysteine levels in both blood and brain. Researchers hypothesized that the increased homocysteine levels in the brain damaged nerve cells in the hippocampus. The mice on the folate diet also experienced DNA damage to hippocampus brain cells because of the Alzheimer's-like plaque, but they were able to repair the DNA damage. The folate-deficient rats, however, incurred hippocampus damage but did not demonstrate the ability to repair cell DNA damage.

Based on this and other emerging research, Mattson speculated that adequate amounts of dietary folic acid could protect brain cells during the aging process, thereby staving off Alzheimer's and other neurodegenerative diseases.


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