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- W2074506871 abstract "Neurodegeneration results from abnormalities in cerebral metabolism and energy balance within neurons, astrocytes, microglia, or microvascular endothelial cells of the blood-brain barrier. In Alzheimer's disease, -amyloid is considered the primary contributor to neuropathology and neurodegeneration. It now is believed that certain systemic diseases, such as diabetes mellitus, can contribute to neurodegeneration through the effects of chronic hyperglycemia/insulin resistance resulting in protein glycation, oxidative stress and inflammation within susceptible brain regions. Here, we present an overview of research focusing on the role of protein glycation, oxidative stress, and inflammation in the neurodegenerative process. Of special interest in this paper is the effect of methylglyoxal (MGO), a cytotoxic byproduct of glucose metabolism, elevated in neurodegenerative disease, and diabetes mellitus, on cerebral protein function and oxidative stress. How MGO interacts with amino acid residues within -amyloid, and small peptides within the brain, is also discussed in terms of the affect on protein function." @default.
- W2074506871 created "2016-06-24" @default.
- W2074506871 creator A5005907143 @default.
- W2074506871 creator A5021420538 @default.
- W2074506871 creator A5045932216 @default.
- W2074506871 date "2011-01-01" @default.
- W2074506871 modified "2023-10-14" @default.
- W2074506871 title "Protein Modification by Dicarbonyl Molecular Species in Neurodegenerative Diseases" @default.
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- W2074506871 doi "https://doi.org/10.4061/2011/461216" @default.
- W2074506871 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3276062" @default.
- W2074506871 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22332001" @default.
- W2074506871 hasPublicationYear "2011" @default.
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