In a study released today at the 2004 AAAS (Triple-A-S) Annual Meeting in Seattle, and published online in the Proceedings of the National Academy of Sciences, scientists with the National Institute on Aging (NIA) suggest that alterations in fats--particularly cholesterol and ceramide--may contribute to a "neurodegenerative cascade" that destroys neurons in Alzheimer's disease. Further, the researchers suggest that the oxidative stress brought on by the presence of the toxic beta amyloid peptide seems to trigger the accumulation of ceramide and cholesterol. The ceramide in turn may trigger the death of nerve cells, the NIA's Mark P. Mattson said.
Lipids (fats) have been implicated in Alzheimer's disease, but only recently have researchers begun to understand their role, and their relationship to the beta amyloid that accumulates in the brains of people with the devastating neurodegenerative disease.
"We had suspected that changes in fat metabolism in the membranes of nerve cells played a role in Alzheimer's but we had not been able to establish a direct link," Mattson said. "With this study, we have been able to illustrate how alterations in membrane lipids can lead to neuronal dysfunction and death."
The new findings also provide an explanation for how antioxidants such as vitamin E might delay the onset of Alzheimer's, suggesting possible new directions for treatment of the disease: The NIA team first established that levels of ceramide and cholesterol were increased in brain cells from deceased Alzheimer's patients. They then found that beta amyloid beta peptide increases ceramide and cholesterol levels in cultured rat nerve cells, and that treatment with
Contact: Monica Amarelo
American Association for the Advancement of Science