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Amyloid β-peptide (1-42)-induced oxidative stress in Alzheimer disease: importance in disease pathogenesis and progression.
TLDR
The signatures of oxidatively modified brain proteins, identified using redox proteomics approaches, during the progression of AD are discussed, with the notion that methionine present at 35 position of Aβ is critical to Aβ-induced oxidative stress and neurotoxicity.
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Identification of nitrated proteins in Alzheimer's disease brain using a redox proteomics approach
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Proteomic identification of oxidized mitochondrial proteins following experimental traumatic brain injury.
TLDR
It is demonstrated that, following TBI, several proteins involved in mitochondrial bioenergetics are highly oxidatively modified, which may possibly underlie the massive breakdown of mitochondrial energetics and eventual cell death known to occur in this model.
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Distribution, elimination, and biopersistence to 90 days of a systemically introduced 30 nm ceria-engineered nanomaterial in rats.
TLDR
The results support concern about the long-term fate and adverse effects of inert nanoscale metal oxides that distribute throughout the body, are persistently retained, and produce adverse changes.
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Lipid peroxidation triggers neurodegeneration: a redox proteomics view into the Alzheimer disease brain.
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Oxidative stress in Alzheimer's disease brain: new insights from redox proteomics.
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Lipopolysaccharide alters the blood–brain barrier transport of amyloid β protein: A mechanism for inflammation in the progression of Alzheimer’s disease
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Adriamycin-induced, TNF-α-mediated central nervous system toxicity
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An increase in S‐glutathionylated proteins in the Alzheimer's disease inferior parietal lobule, a proteomics approach
TLDR
It is demonstrated that specific proteins are sensitive to S‐glutathionylation, which most likely is due to their sensitivity to cysteine oxidation initiated by the increase in oxidative stress in the AD brain.
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Adriamycin-induced, TNF-alpha-mediated central nervous system toxicity.
TLDR
It is demonstrated that ADR autofluorescence was detected only in areas of the brain located outside the blood-brain barrier, but a strong tumor necrosis factor alpha immunoreactivity was detected in the cortex and hippocampus of ADR-treated mice, consistent with the notion that TNF is an important mediator by which ADR induces central nervous system (CNS) injury.
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