Evidence of oxidative damage in Alzheimer's disease brain: central role for amyloid beta-peptide.

By D. Allan Butterfield, J. Drake, C. Pocernich, Alessandra Castegna. Trends in Molecular Medicine, 2001

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Proteomic identification of oxidatively modified proteins in Alzheimer's disease brain. Part II: dihydropyrimidinase‐related protein 2, α‐enolase and heat shock cognate 71 (2002, background): “Several studies demonstrated that brain protein oxidation occurs in AD (Hensley et al. 1995; Markesbery 1997; Butterfield et al. 2001), indicating a role for protein alterations in the processes of neuronal defects associated with AD.”
Amyloid β-peptide (1-42)-induced Oxidative Stress and Neurotoxicity: Implications for Neurodegeneration in Alzheimer's Disease Brain. A Review (2002, neutral): “A Review*”
Environmental pollutants as risk factors for neurodegenerative disorders: Alzheimer and Parkinson diseases (2015, background): “In addition, micromolar concentrations of Aβ induce the formation of H2O2 in culture cells leading to neurotoxicity, and the presence of some antioxidant enzymes prevents the toxicity of the peptide (Butterfield et al., 2001).”
Evidence that amyloid beta-peptide-induced lipid peroxidation and its sequelae in Alzheimer's disease brain contribute to neuronal death. (2002, background): “The centrality of the 42-amino acid form of this peptide, A (1–42), to the pathogenesis of AD was coupled to the extensive oxidative stress under which the AD brain exists in the A -associated free radical oxidative stress model for neurodegeneration in AD brain [14,96].”