Sporadic Alzheimer's Disease: A Bioenergetic Etiology
More than 200 human trials conducted over the last decade have been unable to identify an effective treatment for Alzheimer's disease. "Sporadic Alzheimer's Disease: A Bioenergetic Etiology?" seeks to identify Alzheimer's disease risk mechanisms that would allow prevention and early intervention, which are critical amid the continuing clinical failures in the search for an effective treatment.
Age, sex and apolipoprotien E (APOE) genetic status have been established as the most potent and interrelated triad of risk factors for the development of late-onset sporadic Alzheimer's disease, which accounts for 95 percent of all current Alzheimer's disease cases. In particular, women have a higher lifetime risk of developing sporadic Alzheimer's disease and represent more than two-thirds of the current sporadic Alzheimer's disease population. However, the molecular bases that underlie age-sex-APOE-mediated combined risks for sporadic Alzheimer's disease are unknown.
"Sporadic Alzheimer's Disease: A Bioenergetic Etiology?" is structured to investigate how these risk factors collectively modulate brain metabolic and synaptic activity, which are the two major areas most significantly affected in the preclinical development of Alzheimer's disease. Specifically, research efforts are directed toward understanding the bioenergetic roles in the onset of changes in amyloid homeostasis and synaptic transmission that ultimately result in the development of sporadic Alzheimer's disease.
These studies may lead to critical insights into the etiology, or causes, of Alzheimer's disease and new directions for therapeutic strategies aimed at Alzheimer's prevention, risk reduction, or early intervention.
Image credit: Synapse, Institute on Aging/National Institutes of Health
Department of Pharmacology & Toxicology
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University of Kansas
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