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Nature Medicine 14, 1020 - 1021 (2008)
doi:10.1038/nm1008-1020
Portal to Alzheimer's disease
Anatoly A Starkov1 & Flint M Beal2
- Anatoly A. Starkov is in the Department of Neurology and Neuroscience, Weill Medical College of Cornell University, A501 525 East 68th Street, New York, New York 10065, USA.
e-mail: ans2024@med.cornell.edu - Flint M. Beal is in the Department of Neurology and Neuroscience, Weill Medical College of Cornell University, F610, 1300 York Avenue, New York, New York 10065, USA.
Abstract
Genetic inactivation of the mitochondrial self-destruction mechanism improves cognition in a mouse model of Alzheimer's disease (pages 1097–1105).
Ample evidence suggests that a key event in the etiology of Alzheimer's disease is the excessive production of 
amyloid peptide (A) and its extracellular deposition; deregulation of neuronal metabolism and signaling cascades ensues1. Large A aggregates, also called fibrils, form characteristic amyloid plaques in the brains of individuals with Alzheimer's disease.
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