The research, conducted jointly by USF and the Byrd Institute, is published in the October 2004 issues of the Journal of Alzheimer's Disease and the Neurobiology of Aging.
Previous work has shown that the inflammatory protein ApoE can speed the buildup in the brain of amyloid plaques, the major pathological hallmark of Alzheimer's disease. These deposits of plaques are composed primarily of the amyloid-beta protein (AB). However, the mechanism by which ApoE exerted its ill effects on Alzheimer's disease was unclear.
In the first paper*, published in the Journal of Alzheimer's Disease, the USF/Byrd Institute team found that ApoE is responsible for converting harmless AB into the toxic fibrous deposits, known as filamentous amyloid. The researchers showed that mice with ApoE possessed 3200 times more filamentous amyloid than those without the gene. Diffuse deposits of AB can occur in the elderly in the absence of Alzheimer's disease, and are thought to be a normal aspect of aging, while filamentous amyloid is a toxic product of Alzheimer's disease.
In the second paper**, published in the Neurobiology of Aging, the researchers indicate that the process of altering AB from its diffuse form into filamentous amyloid is needed to damage nerve cells in parts of the brain controlling memory and cognition. Mice with Alzheimer's disease showed memory deficits only when the ApoE gene was present.
"The implication of these studies is that the amyloid promoting activity of ApoE is essential for the development of both Alzheimer's pathology and cognitive decli
Contact: Anne DeLotto Baier
University of South Florida Health