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Lipid peroxidation triggers neurodegeneration: a redox proteomics view into the Alzheimer disease brain.
TLDR
By comparing results obtained at different stages of the AD, it may be possible to identify key biochemical pathways involved and ideally identify therapeutic targets to prevent, delay, or treat AD. Expand
Oxidative stress in Alzheimer's disease brain: new insights from redox proteomics.
TLDR
The application of redox proteomics for the identification of oxidatively modified proteins in Alzheimer's disease brain and the functions associated with the identified oxidized proteins in relation to Alzheimer’s disease pathology are discussed. Expand
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. Expand
Redox proteomic identification of 4-Hydroxy-2-nonenal-modified brain proteins in amnestic mild cognitive impairment: Insight into the role of lipid peroxidation in the progression and pathogenesis of
TLDR
It is suggested that impairment of target proteins through the production of HNE adducts leads to protein dysfunction and eventually neuronal death, thus contributing to the biological events that may lead MCI patients to progress to AD. Expand
Elevated protein-bound levels of the lipid peroxidation product, 4-hydroxy-2-nonenal, in brain from persons with mild cognitive impairment
TLDR
It is shown for the first time in brain obtained at short postmortem intervals that the levels of HNE are elevated in mild cognitive impairment (MCI) hippocampus and inferior parietal lobules compared to those of control brain, suggesting that the pharmacologic intervention to prevent lipid peroxidation at the MCI stage or earlier may be a promising therapeutic strategy to delay or prevent progression to AD. Expand
Tyrosinase protects human melanocytes from ROS-generating compounds.
TLDR
Taken together, data suggest that tyrosinase represents an outstanding protective mechanism against ROS-generating compounds, once primary detoxifying mechanisms are impaired or not available. Expand
Proteomic Analysis of Protein Expression and Oxidative Modification in R6/2 Transgenic Mice
TLDR
It is demonstrated that the expression levels of dihydrolipoamide S-succinyltransferase and aspartate aminotransferase increase consistently over the course of disease (10-week-old mice) and the results for the first time identify specific oxidatively modified proteins that potentially contribute to the pathogenesis of Huntington disease. Expand
Elevated levels of 3-nitrotyrosine in brain from subjects with amnestic mild cognitive impairment: Implications for the role of nitration in the progression of Alzheimer's disease
TLDR
It is demonstrated using slot blot thatprotein nitration is higher in the inferior parietal lobule and hippocampus in MCI compared to those regions from control subjects, and that protein nitration may be important for conversion of MCI to AD. Expand
Oxidatively modified proteins in Alzheimer’s disease (AD), mild cognitive impairment and animal models of AD: role of Abeta in pathogenesis
TLDR
Aβ models of AD strongly support the notion that oxidative stress induced by Aβ may be a driving force in AD pathogenesis, and redox proteomics identified oxidatively modified proteins in AD, MCI and AD models are summarized. Expand
mTOR signaling in aging and neurodegeneration: At the crossroad between metabolism dysfunction and impairment of autophagy
TLDR
The main regulatory roles of mTOR signalling in the brain are discussed, in particular focusing on autophagy, glucose metabolism and mitochondrial functions, which are key players in age-related cognitive decline such as development of Alzheimer disease. Expand
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