The Emerging Link between O-GlcNAc and Alzheimer Disease
Open accessAbstract
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-β 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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Tau undergoes both N-linked glycosylation and O-linked N-acetylglucosaminylation (O-GlcNAcylation), which have been proposed to affect tau phosphorylation and aggregation.
“In addition, tau also undergoes both N-linked glycosylation (N-glycosylation) [171] and O-linked N-acetylglucosaminylation (O-GlcNAcylation) [172], which have been proposed to affect tau phosphorylation and aggregation [173].”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [172]
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References 102 · Cited by 267
- Authors
- Zhu, Y., Shan, X., Yuzwa, S. A., & Vocadlo, D. J.
- Affiliations
- Simon Fraser University (CA)
- Corresponding author
- Vocadlo, David J.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2014-12
- Volume
- 289
- Issue
- 50
- Pages
- 34472-34481
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC4263855
- OpenAlex
- W2004373930
- Cited by
- 267
- References
- 102
- Citations by year
- 2026: 15 · 2025: 18 · 2024: 25 · 2023: 25 · 2022: 21 · 2021: 25 · 2020: 17 · 2019: 26 · 2018: 27 · 2017: 29 · 2016: 24 · 2015: 11 · 2014: 3
- FWCI
- 2.61
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Alzheimer Society
- Canada Research Chairs
- Canadian Institutes of Health Research (MOP 275394)
- Natural Sciences and Engineering Research Council of Canada
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Glycosylation and Glycoproteins Research
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- O-GlcNAc, O-GlcNAcylation, Alzheimer's disease, glucose hypometabolism, tau protein, amyloid precursor protein, amyloid-beta toxicity, neuroprotection, neurodegeneration, post-translational modification, brain glucose metabolism
- MeSH terms
- Acetylglucosamine, Alzheimer Disease, Animals, Glucose, Humans, Neurons, Amyloid beta-Peptides, tau Proteins
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