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Science 324 (5927): 603-604

Copyright © 2009 by the American Association for the Advancement of Science

Medicine

Avoiding Unintended Toxicity

Todd E. Golde, and Thomas L. Kukar

Amyloid-β protein (Aβ) deposition in the brain is one of the pathological hallmarks of Alzheimer's disease. Considerable data support the concept that the aggregation and accumulation of Aβ in the brain trigger a complex pathological cascade that ultimately results in neuronal dysfunction and neurodegeneration (1). Thus, therapies for Alzheimer's disease have focused mainly on preventing or slowing Aβ aggregation, neutralizing toxic Aβ aggregates, or clearing and breaking up these aggregates (2). On page 639 of this issue, Serneels et al. (3) report a theoretically safe approach to decrease Aβ production and thereby slow Aβ aggregation.

Mayo Clinic, College of Medicine, Department of Neuroscience, Mayo Clinic Florida, 4500 San Pablo Road, Jacksonville, FL 32224, USA.

E-mail: tgolde{at}mayo.edu; kukar.thomas{at}mayo.edu


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Lysine 624 of the Amyloid Precursor Protein (APP) Is a Critical Determinant of Amyloid {beta} Peptide Length: SUPPORT FOR A SEQUENTIAL MODEL OF {gamma}-SECRETASE INTRAMEMBRANE PROTEOLYSIS AND REGULATION BY THE AMYLOID {beta} PRECURSOR PROTEIN (APP) JUXTAMEMBRANE REGION.
T. L. Kukar, T. B. Ladd, P. Robertson, S. A. Pintchovski, B. Moore, M. A. Bann, Z. Ren, K. Jansen-West, K. Malphrus, S. Eggert, et al. (2011)
J. Biol. Chem. 286, 39804-39812
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