SOD1 (Copper/Zinc Superoxide Dismutase) Deficiency Drives Amyloid β Protein Oligomerization and Memory Loss in Mouse Model of Alzheimer Disease
Open Access
- 1 December 2011
- journal article
- Published by Elsevier in Journal of Biological Chemistry
- Vol. 286 (52), 44557-44568
- https://doi.org/10.1074/jbc.m111.279208
Abstract
No abstract availableKeywords
This publication has 72 references indexed in Scilit:
- Monoclonal Antibody Against the Turn of the 42-Residue Amyloid β-Protein at Positions 22 and 23ACS Chemical Neuroscience, 2010
- Oxidative Stress in the Progression of Alzheimer Disease in the Frontal CortexJournal of Neuropathology and Experimental Neurology, 2010
- Amyloid-β and tau synergistically impair the oxidative phosphorylation system in triple transgenic Alzheimer's disease miceProceedings of the National Academy of Sciences, 2009
- Structure–neurotoxicity relationships of amyloid β-protein oligomersProceedings of the National Academy of Sciences, 2009
- A Specific Enzyme-Linked Immunosorbent Assay for Measuring β-Amyloid Protein Oligomers in Human Plasma and Brain Tissue of Patients With Alzheimer DiseaseArchives of Neurology, 2009
- Amyloid-β protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memoryNature Medicine, 2008
- Targeting age-related macular degeneration with Alzheimer’s disease based immunotherapies: Anti-amyloid-β antibody attenuates pathologies in an age-related macular degeneration mouse modelVision Research, 2008
- Elevated oxidative stress in erythrocytes due to a SOD1 deficiency causes anaemia and triggers autoantibody productionBiochemical Journal, 2007
- Drusen, choroidal neovascularization, and retinal pigment epithelium dysfunction in SOD1-deficient mice: A model of age-related macular degenerationProceedings of the National Academy of Sciences, 2006
- Neurodegenerative diseases and oxidative stressNature Reviews Drug Discovery, 2004