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Toward a Molecular Etiology of Alzheimer's Disease

Published online by Cambridge University Press:  07 January 2005

Carl Banner
Affiliation:
Neuroscience and Neuropsychology of Aging, National Institute on Aging, Bethesda, Maryland

Abstract

Recent progress in the biochemical characterization of Alzheimer's disease (AD) neuropathology has led to the proposal of three hypotheses for the molecular etiology of AD. One focuses on calcium-activated neutral proteases or calpains (Nixon, 1989). Another focuses on protein phosphorylation (Saitoh & Iimoto, 1989). A third is centered on altered phospholipid metabolism (Pettegrew, 1989). Interestingly, all three hypotheses are mutually compatible, involving closely interlocking biochemical systems. Disturbances in any one of these systems might result in the same type of neuropathology, consistent with suggestions that AD could have multiple etiologies. Future investigations of the function and interrelation of these systems in the central nervous system in general and at the synaptic junction in particular are likely to have significant bearing on our understanding of AD.

Type
Research and Reviews
Copyright
© 1990 Springer Publishing Company

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