Alzheimer’s amyloid β-peptide (1–42): involvement of methionine residue 35 in the oxidative stress and neurotoxicity properties of this peptide
- 30 June 2004
- journal article
- review article
- Published by Elsevier in Neurobiology of Aging
- Vol. 25 (5) , 563-568
- https://doi.org/10.1016/j.neurobiolaging.2003.12.027
Abstract
No abstract availableKeywords
This publication has 48 references indexed in Scilit:
- Neurotoxic, Redox-competent Alzheimer's β-Amyloid Is Released from Lipid Membrane by Methionine OxidationJournal of Biological Chemistry, 2003
- Substitution of isoleucine-31 by helical-breaking proline abolishes oxidative stress and neurotoxic properties of Alzheimer’s amyloid β-peptide (1–42)Free Radical Biology & Medicine, 2002
- Lipid peroxidation and protein oxidation in Alzheimer’s disease brain: potential causes and consequences involving amyloid β-peptide-associated free radical oxidative stress 1,2 1Guest Editors: Mark A. Smith and George Perry 2This article is part of a series of reviews on “Causes and Consequences of Oxidative Stress in Alzheimer’s Disease.” The full list of papers may be found on the homepage of the journal.Free Radical Biology & Medicine, 2002
- Oxidation of Methionine 35 Attenuates Formation of Amyloid β-Peptide 1–40 OligomersJournal of Biological Chemistry, 2002
- Apolipoprotein E modulates Alzheimer’s Aβ(1–42)-induced oxidative damage to synaptosomes in an allele-specific mannerBrain Research, 2002
- Evidence of oxidative damage in Alzheimer's disease brain: central role for amyloid β-peptideTrends in Molecular Medicine, 2001
- Solution structures of micelle-bound amyloid β-(1-40) and β-(1-42) peptides of Alzheimer’s disease 1 1Edited by P. E. WrightJournal of Molecular Biology, 1999
- Solution Structure of Amyloid β-Peptide(1−40) in a Water−Micelle Environment. Is the Membrane-Spanning Domain Where We Think It Is?,Biochemistry, 1998
- Oxidative Stress Hypothesis in Alzheimer's DiseasePublished by Elsevier ,1998
- Deficient glutamate tranport is associated with neurodegeneration in Alzheimer's diseaseAnnals of Neurology, 1996