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Redox proteomics identification of oxidized proteins in Alzheimer's disease hippocampus and cerebellum: An approach to understand pathological and biochemical alterations in AD
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Oxidative modification and down-regulation of Pin1 in Alzheimer's disease hippocampus: A redox proteomics analysis
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Proteomics analysis of the Alzheimer's disease hippocampal proteome.
TLDR
The present study used two-dimensional gel electrophoresis and mass spectrometry techniques to determine changes in protein levels in AD and control hippocampus and identified 18 proteins with altered protein levels that are involved in regulating different cellular functions.
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Amyloid β‐Peptide(1‐42) Contributes to the Oxidative Stress and Neurodegeneration Found in Alzheimer Disease Brain
TLDR
The role of Aβ1–42 in the lipid peroxidation and protein oxidation evident inAD brain and the implications of such oxidative stress for the function of various proteins that have been identified as specifically oxidized in AD brain compared to control, using proteomics methods are discussed.
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Nitric oxide and cellular stress response in brain aging and neurodegenerative disorders: the role of vitagenes.
TLDR
An amount of experimental evidence indicates that increased rate of free radical generation and decreased efficiency of the reparative/degradative mechanisms are factors that primarily contribute to age-related elevation in the level of oxidative stress and brain damage.
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The critical role of methionine 35 in Alzheimer's amyloid beta-peptide (1-42)-induced oxidative stress and neurotoxicity.
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Role of phenylalanine 20 in Alzheimer's amyloid beta-peptide (1-42)-induced oxidative stress and neurotoxicity.
TLDR
Results suggest that long distance electron transfer from methionine 35 through phenylalanine 20 may not play a pivotal role in Abeta(1-42)-mediated oxidative stress and neurotoxicity.
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Proteomics in Alzheimer's disease: insights into potential mechanisms of neurodegeneration
TLDR
This review surveys the proteomics studies relevant to AD, from which new understandings of the pathology, biochemistry, and physiology of AD are beginning to emerge.
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Oxidative Stress, Amyloid-β Peptide, and Altered Key Molecular Pathways in the Pathogenesis and Progression of Alzheimer’s Disease
TLDR
It is opine that targeting altered pathways secondary to oxidative damage in brain from persons with AD, aMCI, or Down syndrome with AD may provide strategies to slow or perhaps one day, prevent, progression or development of this devastating dementing disorder.
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Proteomic identification of proteins specifically oxidized by intracerebral injection of amyloid β-peptide (1–42) into rat brain: Implications for Alzheimer’s disease
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