Bernhard H Moniena, Liana G Apostolovab & Gal Bitan*ca Department of Neurology, David Geffen School of Medicine, University of California at Los Angeles, Neuroscience Research Building 1, Room 455, 635 Charles E. Young Drive South Los Angeles, CA 90095–7334, USA. b Tichi Wilkerson-Kassel Dementia Scholar; UCLA Alzheimer’s Disease Center; 01911 Weyburn Ave., 2nd Floor, Los Angles, CA 90095–7226, USA. c Department of Neurology, David Geffen School of Medicine, University of California at Los Angeles, Neuroscience Research Building 1, Room 451, 635 Charles E. Young Drive South, Los Angeles, CA 90095–7334, USA. † Author for correspondenceAlzheimer’s disease (AD) is a major threat for the rapidly aging world population. AD is the leading cause of dementia and a major cause of death in developed countries. The disease puts a tremendous practical, emotional and financial burden on individuals and governments. Clinicians and researchers in the AD field face great challenges: the pathophysiological processes that cause AD are not well understood, definite diagnosis of AD requires autopsy, and therapeutic options are limited to treating the symptoms rather than the cause of the disease. Nevertheless, new insights into the earliest events that lead to development of AD increase hope that reliable diagnostics and efficacious therapies may emerge.
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Monien et al. (2006) studied this question.
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