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- W2440371497 abstract "Alzheimer disease (AD) is a progressive neurodegenerative disease that affects the elderly population with complex etiology. Many hypotheses have been proposed to explain different causes of AD, but the exact mechanisms remain unclear. In this review, we focus attention on the oxidative-stress hypothesis of neurodegeneration and we discuss redox proteomics approaches to analyze post-mortem human brain from AD brain. Collectively, these studies have provided valuable insights into the molecular mechanisms involved both in the pathogenesis and progression of AD, demonstrating the impairment of numerous cellular processes such as energy production, cellular structure, signal transduction, synaptic function, mitochondrial function, cell cycle progression, and degradative systems. Each of these cellular functions normally contributes to maintain healthy neuronal homeostasis, so the deregulation of one or more of these functions could contribute to the pathology and clinical presentation of AD. In particular, we discuss the evidence demonstrating the oxidation/dysfunction of a number of enzymes specifically involved in energy metabolism that support the view that reduced glucose metabolism and loss of ATP are crucial events triggering neurodegeneration and progression of AD." @default.
- W2440371497 created "2016-06-24" @default.
- W2440371497 creator A5008788895 @default.
- W2440371497 creator A5039202201 @default.
- W2440371497 creator A5042169645 @default.
- W2440371497 creator A5048379669 @default.
- W2440371497 date "2017-07-01" @default.
- W2440371497 modified "2023-10-12" @default.
- W2440371497 title "Oxidative stress, protein modification and Alzheimer disease" @default.
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- W2440371497 doi "https://doi.org/10.1016/j.brainresbull.2016.06.005" @default.
- W2440371497 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27316747" @default.
- W2440371497 hasPublicationYear "2017" @default.
- W2440371497 type Work @default.