| Literature DB >> 12456052 |
G Perry1, A Nunomura, A D Cash, M A Taddeo, K Hirai, G Aliev, J Avila, T Wataya, S Shimohama, C S Atwood, M A Smith.
Abstract
Over the past decade, oxidative stress has been established as the earliest cytological feature of Alzheimer disease and an attractive therapeutic target. The major challenges now are establishing the source of the reactive oxygen and what oxidative stress tells us about the etiology of Alzheimer disease. These are complex issues since a variety of enzymatic and non-enzymatic processes are involved in reactive oxygen formation and damage to macromolecules. In this review, we consider disease mechanisms that show the greatest promise for future research.Entities:
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Year: 2002 PMID: 12456052 DOI: 10.1007/978-3-7091-6139-5_7
Source DB: PubMed Journal: J Neural Transm Suppl ISSN: 0303-6995