Journal
ALZHEIMERS & DEMENTIA
Volume 12, Issue 10, Pages 1078-1089Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jalz.2016.02.011
Keywords
Alzheimer's disease; O-GlcNAcylation; Tau; Hyperphosphorylation; Neurodegeneration
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O-GlcNAcylation is the posttranslational modification of intracellular proteins by O-linked beta-N-acetylglucosamine (O-GlcNAc). The discovery of O-GlcNAc modification of tau and its impact on tau phosphorylation has attracted recent research interest in O-GlcNAc studies in the Alzheimer's disease (AD) field. Modification of proteins by O-GlcNAc occurs extensively in the brain. The expressions and activities of the enzymes catalyzing O-GlcNAc cycling are several-fold higher in the brain than in the peripheral tissues. The O-GlcNAcylation levels of brain proteins including tau are decreased in AD brain, probably due to decreased brain glucose metabolism. The reduction of brain O-GlcNAcylation appears to mediate the molecular mechanism by which decreased brain glucose metabolism contributes to neurodegeneration. Studies on mouse models of tauopathies suggest a neuroprotective role of pharmacological elevation of brain O-GlcNAc, which could potentially be a promising approach for treating AD and other neurodegenerative diseases. (C) 2016 The Alzheimer's Association. Published by Elsevier Inc. All rights reserved.
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