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A model for beta-amyloid aggregation and neurotoxicity based on free radical generation by the peptide: relevance to Alzheimer disease.
TLDR
Evidence is presented that beta-amyloid fragments, at concentrations that previously have been shown to be neurotoxic to cultured neurons, can inactivate oxidation-sensitive glutamine synthetase and creatine kinase enzymes and generate free radical peptides.
Review: Alzheimer's amyloid beta-peptide-associated free radical oxidative stress and neurotoxicity.
TLDR
Significant evidence is outlined from multiidisciplinary approaches for amyloid beta-peptide-associated free radical oxidative stress and neurotoxicity and protection against these oxidative processes and cell death by free radical scavengers and the strong evidence supporting the notion that the single methionine residue of amyloids beta- peptide is vital to the oxidative Stress and neurotoxicological properties of this peptide.
Oxidative Modification of Creatine Kinase BB in Alzheimer’s Disease Brain
TLDR
The analysis of specific protein carbonyl levels in CK BB, performed by two‐dimensional fingerprinting of oxidatively modified proteins, identified CK BB as one of the targets of protein oxidation in the AD brain.
Different Mechanisms of Oxidative Stress and Neurotoxicity for AlzheimersA ‚(1-42) and A‚(25-35)
TLDR
These studies reveal that two different mechanisms may be operative in the two peptides; however, the single methionine residue in the peptides appears to play a crucial role in both mechanisms.
Different mechanisms of oxidative stress and neurotoxicity for Alzheimer's A beta(1--42) and A beta(25--35).
TLDR
These studies reveal that two different mechanisms may be operative in the two peptides; however, the single methionine residue in the peptides appears to play a crucial role in both mechanisms.
Brain Regional Correspondence Between Alzheimer's Disease Histopathology and Biomarkers of Protein Oxidation
TLDR
The brain regional variation of these oxidation‐sensitive biomarkers corresponds to established histopathological features of AD and is paralleled by an increase in immunoreactive microglia, indicating that senile plaque‐dense regions of the AD brain may represent environments of elevated oxidative stress.
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