Literature DB >> 25336656

The emerging link between O-GlcNAc and Alzheimer disease.

Yanping Zhu1, Xiaoyang Shan2, Scott A Yuzwa2, David J Vocadlo3.   

Abstract

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.
© 2014 by The American Society for Biochemistry and Molecular Biology, Inc.

Entities:  

Keywords:  Alzheimer Disease; Amyloid-β (Aβ); Brain Metabolism; Glucose Metabolism; Glycobiology; Glycoprotein; Glycosylation; O-GlcNAcylation; O-Linked N-Acetylglucosamine (O-GlcNAc); Tau Protein (Tau)

Mesh：

Substances：

Year:  2014        PMID： 25336656      PMCID： PMC4263855          DOI： 10.1074/jbc.R114.601351

Source DB:  PubMed          Journal:  J Biol Chem        ISSN： 0021-9258            Impact factor:   5.157


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