Alzheimer's Disease

Edited by: Paul Smaglik M. Citron, D. Westaway, W.M. Xia, G. Carlson, T. Diehl, G. Levesque, K. Johnson-Wood, M. Lee, P. Seubert, A. Davis, D. Kholodenko, R. Motter, R. Sherrington, B. Perry, H. Yao, R. Strome, I. Lieberburg, J. Rommens, S. Kim, D. Schenk, P. Fraser, P.S. Hyslop, D.J. Selkoe, "Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid ß protein in both transfected cells and transgenic mice, Nature Medicine, 3:67-72, January 1997. (Cited in more th

The Scientist Staff
Sep 12, 1999

Edited by: Paul Smaglik
M. Citron, D. Westaway, W.M. Xia, G. Carlson, T. Diehl, G. Levesque, K. Johnson-Wood, M. Lee, P. Seubert, A. Davis, D. Kholodenko, R. Motter, R. Sherrington, B. Perry, H. Yao, R. Strome, I. Lieberburg, J. Rommens, S. Kim, D. Schenk, P. Fraser, P.S. Hyslop, D.J. Selkoe, "Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid ß protein in both transfected cells and transgenic mice, Nature Medicine, 3:67-72, January 1997. (Cited in more than 200 papers since publication).

Comments by Dennis J. Selkoe, professor of neurology and neuroscience, Center for Neurologic Diseases, Harvard Medical School and Brigham and Women's Hospital

Neurobiologists studying Alzheimer's disease agree that plaque deposits in the brain serve as significant signposts on the disease progression pathway. However, opinions differ as to whether those plaques--largely composed of amyloid ß proteins--cause the disease or are merely an effect of it. Dennis J....

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