Reduced antioxidant enzyme activity in brains of mice transgenic for human presenilin-1 with single or multiple mutations

  • Alzheimer's disease-related mutations in the presenilin-1 gene (PS1) are leading to an elevated production of neurotoxic beta-amyloid 1-42 and may additionally enhance oxidative stress. Here, we provide in vivo evidence indicating that brains of transgenic mice expressing different human Alzheimer-linked PS1 mutations exhibit a reduced activity of two antioxidant enzymes. For this purpose, mice transgenic for human PS1 and for single and multiple PS1 mutations were generated. Mice with multiple PS1 mutations showed a significantly decreased activity of the antioxidant enzymes Cu/Zn superoxide dismutase and glutathione reductase already at an age of 3-4 months. As expected, this effect was less pronounced for the mice with a single PS1 mutation. By contrast, animals bearing normal human PS1 showed significantly elevated enzyme activities relative to non-transgenic littermate controls.

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Author:Silke LeutnerGND, Christian CzechORCiD, Katharina SchindowskiORCiDGND, Nathalie Touchet, Anne EckertORCiDGND, Walter E. MüllerGND
Parent Title (English):Neuroscience letters : an international multidisciplinary journal devoted to the rapid publication of basic research in the neurosciences
Publisher:Elsevier Science
Place of publication:Amsterdam [u.a.]
Document Type:Article
Date of Publication (online):2006/12/06
Year of first Publication:2000
Publishing Institution:Universitätsbibliothek Johann Christian Senckenberg
Release Date:2006/12/06
Tag:Alzheimer's disease; Glutathione reductase; Lipid peroxidation; Presenilin; Reactive oxygen species; Superoxide dismutase
Issue:2, Oct. 6
Page Number:4
First Page:87
Last Page:90
Institutes:Biochemie, Chemie und Pharmazie / Pharmazie
Dewey Decimal Classification:5 Naturwissenschaften und Mathematik / 57 Biowissenschaften; Biologie / 570 Biowissenschaften; Biologie
Sammlungen:Sammlung Biologie / Sondersammelgebiets-Volltexte
Licence (German):License LogoDeutsches Urheberrecht