ArticleNeurochemical research2002
Oxidative stress in synaptosomal proteins from mutant presenilin-1 knock-in mice: implications for familial Alzheimer's disease.
Article in Neurochemical research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 38 citations in OpenAlex.
- Role of Metal Cations of Copper, Iron, and Aluminum and Multifunctional Ligands in Alzheimer's Disease: Experimental and Computational Insights.ACS omega · 2023Review
- The protective effects of Agomelatine against Aβ1-42 oligomers-induced cellular senescence mediated by SIRT6 and Agomelatine's potential in AD treatment.Human cell · 2021Article
- Increased oxidative stress contributes to enhance brain amyloidogenesis and blunts energy metabolism in sucrose-fed rat: effect of AMPK activation.Scientific reports · 2021Article
- Review
- Brain lipid peroxidation and alzheimer disease: Synergy between the Butterfield and Mattson laboratories.Ageing research reviews · 2020Review
- Article
- Oxidative stress and metabolic syndrome: cause or consequence of Alzheimer's disease?Oxidative medicine and cellular longevity · 2014Review
- 4-Hydroxy-2-nonenal, a reactive product of lipid peroxidation, and neurodegenerative diseases: a toxic combination illuminated by redox proteomics studies.Antioxidants & redox signaling · 2012Review
- Redox proteomics in selected neurodegenerative disorders: from its infancy to future applications.Antioxidants & redox signaling · 2012Review
- Age-related loss of phospholipid asymmetry in APP(NLh)/APP(NLh) x PS-1(P264L)/PS-1(P264L) human double mutant knock-in mice: relevance to Alzheimer disease.Neurobiology of disease · 2010Article
- Presenilin transgenic mice as models of Alzheimer's disease.Brain structure & function · 2010Review
- A new and simple approach for genotyping Alzheimer's disease presenilin-1 mutant knock-in mice.Journal of neuroscience methods · 2009Article
- Molecular pathogenesis of Alzheimer's disease: reductionist versus expansionist approaches.International journal of molecular sciences · 2009Review
- Age-related loss of synaptophysin immunoreactive presynaptic boutons within the hippocampus of APP751SL, PS1M146L, and APP751SL/PS1M146L transgenic mice.The American journal of pathology · 2005Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Presenilin-1 (PS-1) is a transmembrane protein that may be involved in the processing of amyloid precursor protein (APP). Mutations in PS-1 are the major cause of familial Alzheimer's disease (AD). AD brain is under significant oxidative stress, including protein oxidation. In the present study, protein oxidation was compared in synaptosomes from knock-in mice expressing mutant human PS-I (M146V mutation) and from wild-type mice expressing non-mutant human PS-1. Synaptosomal membrane protein conformational alterations associated with oxidative stress were measured using electron paramagnetic resonance (EPR) in conjunction with a protein-specific spin-label. Direct synaptosomal protein oxidation was assessed by a carbonyl detection assay. Synaptosomal proteins from PS-1 mutant mice displayed increased oxidative stress as measured by both techniques, compared with synaptosomal proteins from wild type mice. These data suggest that PS-1 mutations cause oxidative alterations in synaptosomal membrane protein structure and oxidative modification of synaptosomal proteins. Our findings suggest that familial AD may be associated with oxidative stress that may play a pivotal role in neuronal dysfunction and death.
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