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Issue title: Mini-Forum: Roles of Amyloid-β and Tau Phosphorylation in Neuronal Repair and Protection
Article type: Research Article
Authors: Menon, Parekkat M.a; * | Vonsattel, Jean Paulb | Jolles, Paul R.c
Affiliations: [a] Department of Radiology, University of Mississippi Medical Center, Jackson, MS, USA | [b] Taub Institute for Research on Alzheimer Disease and the Aging Brain, Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, NY, USA | [c] Nuclear Medicine Division, Department of Radiology, Virginia Commonwealth University Medical Center, Richmond, VA, USA | Department of Psychiatry and Human Behavior, University of Mississippi Medical Center, Jackson, MS, USA
Correspondence: [*] Corresponding author: Parekkat M. Menon, Department of Radiology, University of Mississippi Medical Center, 2500 North State Drive, Jackson, MS 39216, USA. Tel.: +1 601 815 5615; E-mail: [email protected].
Abstract: Over the past several decades, there has been extensive research devoted toward determining the cause of Alzheimer's disease. Numerous biochemical, histological, and imaging investigations have elegantly characterized the neuropathologic and functional changes associated with AD. Proponents of one theory or another can find supporting data among the myriad of studies in the literature. This paper attempts to summarize some of the major conclusions and controversies in imaging literature (especially, magnetic resonance imaging and nuclear medicine) in relation to pathogenesis theories of Alzheimer's disease. In spite of considerable progress, the primary cause of Alzheimer's disease remains elusive.
Keywords: Amyloid-β, atrophy, MRI, neurodegeneration, PET, tau, vascular
DOI: 10.3233/JAD-2009-1166
Journal: Journal of Alzheimer's Disease, vol. 18, no. 2, pp. 419-427, 2009
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