Folic Acid & Alzheimer’s Disease

More applications of folic acid supplementation are appearing in the research literature.  People who have Alzheimer’s disease, for example, often have low levels of folic acid in their blood. Increasing folic acid intake by supplementation could be beneficial to the aging brain, protecting it against Alzheimer’s and other neurodegenerative diseases. In AD, plaques develop first in areas of the brain that are essential for memory and other cognitive functions. Plaques include deposits of a protein, beta-amyloid. Unlike human brain cells, brain cells in mice are not killed by the progressive accumulation of beta amyloid. According to a press report from the US National Institute of Aging:

“Mouse experiments suggest that folic acid could play an essential role in protecting the brain against the ravages of Alzheimer’s disease and other neurodegenerative disorders, according to scientists at the National Institute on Aging. In one animal study the underlying biochemical mechanisms were investigated: People with high blood levels of homocysteine have nearly twice the risk of developing the disease.

“The NIA team counted neurons in the hippocampus, a brain region critical for learning and memory that is destroyed as plaques accumulate during Alzheimer’s disease (AD). The investigators found a decreased number of neurons in the mice fed the folic acid deficient diet. The scientists also discovered that mice with low amounts of dietary folic acid had elevated levels of homocysteine, an amino acid, in the blood and brain. They suspect that increased levels of homocysteine in the brain caused damage to the DNA of nerve cells in the hippocampus. In transgenic mice fed an adequate amount of folate, nerve cells in this brain region were able to repair damage to their DNA. But in the transgenic mice fed a folate-deficient diet, nerve cells were unable to repair this DNA damage… 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 the NIA’s Laboratory of Neurosciences and the study’s principal investigator. “

Folic Acid Possibly A Key Factor In Alzheimer’s Disease Prevention

I. Kruman, T.S. Kumaravel, A. Lohani, W. Pedersen, R.G. Cutler, Y. Kruman, N. Haughey, J. Lee, M. Evans, and M.P. Mattson, “Folic Acid Deficiency and Homocysteine Impair DNA Repair in Hippocampal Neurons and Sensitize Them To Amyloid Toxicity in Experimental Models of Alzheimer’s Disease,” Journal of Neuroscience, 22:5, pp. 1752-1762.

S. Sesdradri, A. Beiser, J. Selhub, et al., “Plasma Homocysteine As A Risk Factor For Dementia and Alzheimer’s Disease,” N Eng J Med, 346:7, pp. 476-483.

This discussion is continued in

The Book of Brain  and Nutrition Notes .