In the study, published in the March 1, 2002 issue of the Journal of Neuroscience, the investigators fed one group of mice with Alzheimers-like plaques in their brains a diet that included normal amounts of folate, while a second group was fed a diet deficient in this vitamin. . These mice are transgenic, meaning they were bred with mutant genes that cause AD in people. They develop AD-like plaques in their brains that kill neurons.
The NIA team counted neurons in the hippocampus, a brain region critical for learning and memory that is destroyed as plaques accumulate during Alzheimers disease. 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 NIAs Laboratory of Neurosciences
Contact: Doug Dollemore
NIH/National Institute on Aging