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Article type: Review Article
Authors: Sagara, Yutaka | Tan, Shirlee | Maher, Pamela | Schubert, David;
Affiliations: The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA | Scripps Research Institute, 10666 North Torrey Pines Road, La Jolla, CA 92037, USA
Note: [] Correspondence should be sent to: Prof. David Schubert, The Salk Institute for Biological Studies, P.O. Box 85800, San Diego, CA 92186‐5800, USA. Tel.: (619) 453 4100; Fax: (619) 535 9062.
Abstract: It is likely that amyloid \beta‐protein (A\beta) mediates nerve cell death in Alzheimer’s disease (AD). Some nerve cell populations, however, remain undamaged in AD brain. To understand the biochemical basis for resistance to A\beta toxicity, a series of cell lines were isolated which are resistant to A\beta toxicity. It is shown that a major component of the resistance mechanism is the transcriptional elevation of two H_{2}O_{2} degrading enzymes, glutathione peroxidase and catalase. These data support other evidence for the role of oxidative damage in A\beta toxicity, and suggest strategies for clinical approaches to the disease.
Journal: Biofactors, vol. 8, no. 1-2, pp. 45-50, 1998
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