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Excess brain protein oxidation and enzyme dysfunction in normal aging and in Alzheimer disease.

It is concluded that protein oxidation products accumulate in the brain and that oxidation-vulnerable enzyme activities decrease with aging in the same regional pattern (frontal more affected than occipital) and that AD may represent a specific brain vulnerability to age-related oxidation.
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A model for beta-amyloid aggregation and neurotoxicity based on free radical generation by the peptide: relevance to Alzheimer disease.

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.
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Oxidative Alterations in Alzheimer's Disease

Overall these studies indicate that oxidative stress and the inflammatory cascade, working in concert, are important in the pathogenetic cascade of neurodegeneration in AD, suggesting that therapeutic efforts aimed at both of these mechanisms may be beneficial.
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Free radical damage to protein and DNA: Mechanisms involved and relevant observations on brain undergoing oxidative stress

Results show that oxidative damage to brain during aging is decreased by chronic administration of PBN, which may be related to its trapping of specific free radicals, which triggers a cascade of oxidative events that eventually lead to tissue injury.
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Reversal of age-related increase in brain protein oxidation, decrease in enzyme activity, and loss in temporal and spatial memory by chronic administration of the spin-trapping compound…

Oxygen free radicals and oxidative events have been implicated as playing a role in bringing about the changes in cellular function that occur during aging and chronic treatment with the spin-trapping compound PBN caused a decrease in the level of oxidized protein and an increase in both GS and neutral protease activity in aged Mongolian gerbil brain.
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Oxidative damage to brain proteins, loss of glutamine synthetase activity, and production of free radicals during ischemia/reperfusion-induced injury to gerbil brain.

It is reported that free radical flux is increased during the reperfusion phase of the ischemia-lesioned gerbil brain, and the free radical spin trap N-tert-butyl-alpha-phenylnitrone-dependent nitroxide radical obtained in the lipid fraction.
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Brain Regional Correspondence Between Alzheimer's Disease Histopathology and Biomarkers of Protein Oxidation

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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Oxygen free radical involvement in ischemia and reperfusion injury to brain

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3,7-Dimethyl-1-propargylxanthine: a potent and selective in vivo antagonist of adenosine analogs.

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Reactive Oxygen Species as Causal Agents in the Neurotoxicity of the Alzheimer's Disease‐Associated Amyloid Beta Peptide a

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