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Article type: Review Article
Authors: Bredesen, Dale E.a; b; * | John, Varghesea | Galvan, Veronicac
Affiliations: [a] Buck Institute for Age Research, Novato, CA, USA | [b] Department of Neurology, University of California, San Francisco, CA, USA | [c] Department of Physiology and The Sam and Ann Barshop Institute for Longevity and Aging Studies, University of Texas San Antonio Health Science Center, Texas Research Park Campus, San Antonio, TX, USA
Correspondence: [*] Correspondence to: Dale E. Bredesen, Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA. Tel.: +1 415 209 2090; Fax: +1 415 209 2230; E-mail: dbredesen@buckinstitute.org.
Note: [] Handling Associate Editor: James Bamburg
Abstract: Reports from multiple laboratories have now been published analyzing the critical nature of the caspase cleavage site of amyloid-β protein precursor (AβPP) for cell death induction, synaptic loss, hippocampal atrophy, long-term potentiation, memory loss, neophobia, and other aspects of the Alzheimer's phenotype. Here we review the results and implications of these studies for the understanding of Alzheimer's disease pathophysiology and the potential development of therapeutics that target this site in AβPP.
Keywords: Alzheimer's disease, amyloid-β peptide caspases, transgenic mouse
DOI: 10.3233/JAD-2010-100537
Journal: Journal of Alzheimer's Disease, vol. 22, no. 1, pp. 57-63, 2010
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