Affiliations: Departments of Neurology, Neuroscience and Graduate Program in Neuroscience, University of Minnesota, Minneapolis, MN 55455, USA; Geriatric Research, Education and Clinical Center, Minneapolis Veterans Affairs Medical Center, Minneapolis, MN 55417, USA
Correspondence:
[*]
Address for correspondence: Karen H. Ashe, MD, PhD, Department of Neurology, Mayo Mail Code 295, 420 Delaware Street, SE, Minneapolis, MN 55455, USA. Tel.: +1 612 626 0652; Fax: +1 612 626 2639; E-mail: hsiao005@umn.edu.
Abstract: Understanding the pathophysiology and treatment of Alzheimer's disease is vitally important. Alzheimer's disease threatens to affect currently at least 30% of all individuals currently alive in the 12 most financially developed countries, unless interventions are discovered to prevent or treat the disease. Although memory loss is the cardinal symptom of Alzheimer's disease, the pathophysiological mechanisms leading to cognitive deficits are poorly understood. It is difficult to address this problem in human studies, and impossible in cultured cells. Therefore, animal models are needed to elucidate the molecular mechanisms leading to dementia. A large number of animal models have focussed upon the role of amyloid plaques in the pathogenesis of Alzheimer's disease, because amyloid plaques are an essential diagnostic feature of the disease. However, the mechanism by which amyloid plaques or their principal molecular constituent, the amyloid-β protein (Aβ), disrupt cognitive function is not well understood. Herein, I describe my perspective on what we have learned about how Aβ impairs memory from research on Alzheimer's disease in mice and rats.
