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Journal of Biomedicine and Biotechnology
Volume 2006, Article ID 12129, 3 pages
Review Article

Interplay Between Oxidative Damage, Protein Synthesis, and Protein Degradation in Alzheimer's Disease

Anatomy and Neurobiology, Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA

Received 4 November 2005; Revised 31 January 2006; Accepted 1 February 2006

Copyright © 2006 Jeffrey N. Keller. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Protein synthesis and protein degradation are highly regulated cellular processes that are essential to maintaining cell viability. Numerous studies now indicate that protein synthesis and protein degradation are significantly altered in Alzheimer's disease (AD), with impairments in these two processes potentially contributing to AD pathogenesis. Alterations in steady state protein regulation may be a particularly important factor in regulating whether cells maintain homeostasis in response to oxidative damage, or conversely whether oxidative stress is induced by oxidative damage. The focus of this review is to discuss recent findings on each of these topics, and to discuss their importance to the onset and progression of AD.