Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 289, Issue 50, Pages 34472-34481Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.R114.601351
Keywords
Alzheimer Disease; Amyloid- (A); Brain Metabolism; Glucose Metabolism; Glycobiology; Glycoprotein; Glycosylation; O-GlcNAcylation; O-Linked N-Acetylglucosamine (O-GlcNAc); Tau Protein (Tau)
Categories
Funding
- Natural Sciences and Engineering Research Council of Canada
- Canadian Institutes of Health Research [MOP 275394]
- Alzheimer Society of Canada
- Canadian Institutes of Health Research
- Canada Research Chairs Program
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Regional glucose hypometabolism is a defining feature of Alzheimer disease (AD). One emerging link between glucose hypometabolism and progression of AD is the nutrient-responsive post-translational O-GlcNAcylation of nucleocytoplasmic proteins. O-GlcNAc is abundant in neurons and occurs on both tau and amyloid precursor protein. Increased brain O-GlcNAcylation protects against tau and amyloid- peptide toxicity. Decreased O-GlcNAcylation occurs in AD, suggesting that glucose hypometabolism may impair the protective roles of O-GlcNAc within neurons and enable neurodegeneration. Here, we review how O-GlcNAc may link cerebral glucose hypometabolism to progression of AD and summarize data regarding the protective role of O-GlcNAc in AD models.
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