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Article type: Research Article
Authors: Selkoe, Dennis J.
Affiliations: Center for Neurologic Diseases, Harvard Institutes of Medicine, Rm 730, 77 Avenue Louis Pasteur, Boston MA 02115, USA. Tel.: +1 617 525 5200; Fax: +1 617 525 5252; E-mail: dselkoe@rics.bwh.harvard.edu
Abstract: In the twenty years since George Glenner identified the amyloid β-protein (Aβ), advances in understanding the biochemical pathology, genetics and cell biology of Alzheimer's disease have led to a detailed molecular hypothesis for the genesis of AD and brought us into human trials of anti-amyloid agents. The ability to study Aβ dynamically in cultured cells and in vivo derives from the recognition in 1992 that Aβ is a normal product of cellular metabolism throughout life and circulates as a soluble peptide in biological fluids. Here, I review the background underlying this discovery and then discuss its implications for research on Alzheimer's disease, particularly for the development of disease-modifying therapies.
Keywords: Amyloid β-protein, APP, secretases, Alzheimer's disease, drug discovery
DOI: 10.3233/JAD-2006-9S319
Journal: Journal of Alzheimer's Disease, vol. 9, no. s3, pp. 163-168, 2006
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