J. Carney

Publications206
h-index53
Citations13,315
Highly Influential Citations243
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Excess brain protein oxidation and enzyme dysfunction in normal aging and in Alzheimer disease.
TLDR
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. Expand
Oxidative Alterations in Alzheimer's Disease
TLDR
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. Expand
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. Expand
Oxidative damage to brain proteins, loss of glutamine synthetase activity, and production of free radicals during ischemia/reperfusion-induced injury to gerbil brain.
TLDR
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. Expand
Free radical damage to protein and DNA: Mechanisms involved and relevant observations on brain undergoing oxidative stress
TLDR
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. Expand
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…
TLDR
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. Expand
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. Expand
Reactive Oxygen Species as Causal Agents in the Neurotoxicity of the Alzheimer's Disease‐Associated Amyloid Beta Peptide a
Oxygen free radical involvement in ischemia and reperfusion injury to brain
TLDR
Increased levels of DHBA in brain correlated with ischemia reperfusion-mediated behavioral modification of gerbils, but salicylate administration did not protect against the behavior changes. Expand
3,7-Dimethyl-1-propargylxanthine: a potent and selective in vivo antagonist of adenosine analogs.
TLDR
DMPX potently and selectively blocked the actions of the potent A2 adenosine agonist, 5'-N-ethylcarboxamidoadenosine (NECA), in DBA/2 mice, compared to blockade of the same responses elicited by the selective A1-adenosine ligand, N6-cyclohexyladenosines (CHA). Expand
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