What question did this study set out to answer?

To review evidence detailing how amyloid beta-peptide (1-42) promotes free radical oxidative stress and neurodegeneration in Alzheimer's disease brain tissue and experimental models.

January 1, 2002Free Radical Research

Amyloid β-peptide (1-42)-induced Oxidative Stress and Neurotoxicity: Implications for Neurodegeneration in Alzheimer's Disease Brain. A Review

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Authors

DBD. Allan ButterfieldNational Oceanic and Atmospheric Administration

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Implication

Narrative review uncovers molecular mechanisms of amyloid beta neurotoxicity in Alzheimer's disease models, highlighting methionine-driven oxidative stress.

Key Points

To review evidence detailing how amyloid beta-peptide (1-42) promotes free radical oxidative stress and neurodegeneration in Alzheimer's disease brain tissue and experimental models.
Synthesized in vitro and in vivo studies examining structural mutations in amyloid beta-peptide (1-42), focusing on methionine-35, isoleucine-31, and glycine-37 substitutions.
Evaluated synaptosome vulnerability to oxidative stress across wild-type, apoE knock-out, and human apoE targeted replacement (apoE2, apoE3, apoE4) mouse models.
Reviewed proteomic and immunoprecipitation analyses of postmortem human Alzheimer's disease brain tissue (postmortem interval ≤ 4 hours) to identify selectively oxidized proteins.
Mutation of isoleucine-31 to proline or displacement of methionine-35 via glycine-to-aspartate substitution completely abrogated amyloid beta-induced oxidative stress and neurotoxicity, while vitamin E prevented reactive oxygen species formation and neuronal damage.
Brain membranes and synaptosomes expressing human apoE4 exhibited significantly heightened vulnerability to amyloid beta-induced protein oxidation, lipid peroxidation, and reactive oxygen species generation compared to apoE2 and apoE3 models.
Selective oxidative modifications were identified in key brain enzymes, including creatine kinase, beta-actin, and glutamate transporter 1 (Glt-1), directly impairing cellular energy metabolism, cytoskeletal assembly, and glutamate clearance.

Cite This Study

D. Allan Butterfield (2002) studied this question.

synapsesocial.com/papers/6a841d0fd87e21f83cb2935d https://doi.org/10.1080/1071576021000049890

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Implication

Narrative review uncovers molecular mechanisms of amyloid beta neurotoxicity in Alzheimer's disease models, highlighting methionine-driven oxidative stress.

Amyloid β-peptide (1-42)-induced Oxidative Stress and Neurotoxicity: Implications for Neurodegeneration in Alzheimer's Disease Brain. A Review

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Implication

Key Points

Cite This Study

Amyloid β-peptide (1-42)-induced Oxidative Stress and Neurotoxicity: Implications for Neurodegeneration in Alzheimer's Disease Brain. A Review

Discussion

Member takes

Implication

Key Points

Cite This Study

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