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- W2000446523 abstract "Alzheimer disease (AD) is a progressive dementia affecting a large proportion of the aging population. The histopathological changes in AD include neuronal cell death, formation of amyloid plaques and neurofibrillary tangles. There is also evidence that brain tissue in patients with AD is exposed to oxidative stress (e.g., protein oxidation, lipid oxidation, DNA oxidation and glycoxidation) during the course of the disease. Advanced glycation endproducts (AGEs) are present in amyloid plaques in AD, and its extracellular accumulation may be caused by an accelerated oxidation of glycated proteins. AGEs participate in neuronal death causing direct (chemical) and indirect (cellular) free radical production and consequently increase oxidative stress. The development of drugs for the treatment of AD that breaks the vicious cycles of oxidative stress and neurodegeneration offer new opportunities. These approaches include AGE-inhibitors, antioxidants and anti-inflammatory substances, which prevent free radical production." @default.
- W2000446523 created "2016-06-24" @default.
- W2000446523 creator A5020856144 @default.
- W2000446523 creator A5054147471 @default.
- W2000446523 date "2009-01-01" @default.
- W2000446523 modified "2023-10-10" @default.
- W2000446523 title "Oxidative stress in Alzheimer disease" @default.
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- W2000446523 doi "https://doi.org/10.4161/cam.3.1.7402" @default.
- W2000446523 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2675154" @default.
- W2000446523 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19372765" @default.
- W2000446523 hasPublicationYear "2009" @default.
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