Affiliations: [a] Department of Neurology, The Second Hospital of Shanxi Medical University, Taiyuan, China
| [b] Academy of Chinese Medical Science, Henan University of Chinese Medicine, Zhengzhou, China
Correspondence:
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Correspondence to: Guofang Xue, Department of Neurology, The Second Hospital of Shanxi Medical University, No. 382 Wuyi Road, Taiyuan 030001, Shanxi Province, China. Tel.: +86 13546313726; E-mail: xueguofangty@163.com.
Abstract: As a non-classical post-translational modification, O-linked β-N-acetylglucosamine (O-GlcNAc) modification (O-GlcNAcylation) is widely found in human organ systems, particularly in our brains, and is indispensable for healthy cell biology. With the increasing age of the global population, the incidence of neurodegenerative diseases is increasing, too. The common characteristic of these disorders is the aggregation of abnormal proteins in the brain. Current research has found that O-GlcNAcylation dysregulation is involved in misfolding or aggregation of these abnormal proteins to mediate disease progression, but the specific mechanism has not been defined. This paper reviews recent studies on O-GlcNAcylation’s roles in several neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, Huntington’s disease, Machado-Joseph’s disease, and giant axonal neuropathy, and shows that O-GlcNAcylation, as glucose metabolism sensor, mediating synaptic function, participating in oxidative stress response and signaling pathway conduction, directly or indirectly regulates characteristic pathological protein toxicity and affects disease progression. The existing results suggest that targeting O-GlcNAcylation will provide new ideas for clinical diagnosis, prevention, and treatment of neurodegenerative diseases.
