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Article type: Review Article
Authors: Takashima, Akihiko; *
Affiliations: Laboratory for Alzheimer's Disease, RIKEN Brain Science Institute, Wako, Saitama, Japan
Correspondence: [*] Address for correspondence: Akihiko Takashima, Ph.D., Laboratory for Alzheimer's Disease, Brain Science Institute, RIKEN, 2-1 Hirosawa, Wako-shi, Saitama 351-0198, Japan. Tel.: +81 48 467 9704; Fax: +81 48 467 5916; E-mail: [email protected].
Abstract: Alzheimer's disease (AD) is clinically characterized as a progressive dementia starting with memory dysfunction and characterized pathologically as neurodegeneration accompanied by deposition of amyloid-β, neurofibrillary tangles, and neuronal loss. AD research has endeavored to explain the clinical symptoms of AD through pathological changes and to develop various therapies for AD. Fulfillment of these goals, however, remains on the horizon. In this article, I review the relationship between neuropathological changes that occur in the brain and clinical progression of AD, and propose a hypothesis that brain aging, characterized by neurofibrillary tangles in entorhinal cortex, is pre-requisite for development of AD.
Keywords: Amyloid-β, dementia, tau
DOI: 10.3233/JAD-2009-1090
Journal: Journal of Alzheimer's Disease, vol. 17, no. 4, pp. 729-736, 2009
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