ArticleCell death & disease2024
Protective effect of increased O-GlcNAc cycling against 6-OHDA induced Parkinson's disease pathology.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Genome-Wide Meta-Analysis of Parkinson's Disease Associated Genetic Loci and Validation of Therapeutic Targets.Brain and behavior · 2025Pooled it
- O-GlcNAcylation: A molecular switch linking brain health to neurodegeneration.Neural regeneration research · 2026Article
- Brain O-GlcNAcylation in Neurodegenerative Diseases: Context-Dependent Mechanisms and Precision Therapeutic Translation.Brain sciences · 2026Review
- Genetic Rescue of Pathogenic O-GlcNAc Dyshomeostasis Associated with Microcephaly and Motor Deficits.eNeuro · 2026Article
- O-GlcNAcylation reprograms microglial inflammatory states and attenuates Alzheimer's disease pathology.Cell death & disease · 2026Article
- Investigation of the Effects of Saffron on Neuroprotection and Circadian Rhythm in anPharmaceuticals (Basel, Switzerland) · 2026Article
- Spermidine Suppresses Peripheral Inflammation and Alleviates Non-Motor Symptoms in the 6-OHDA-Induced Rat Model of Parkinson's Disease.Molecules (Basel, Switzerland) · 2026Article
- O-GlcNAcylation regulates microglial neuroinflammation in Parkinson's disease.NPJ Parkinson's disease · 2026Article
- Glucosamine as a regulator of O-GlcNAc signaling: linking metabolism to disease pathogenesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Review
- Alloxan attenuates glucosamine-induced NF-κB activation and proinflammatory gene expression under normoglycemic conditions.BMB reports · 2025Article
- Modulation of O-GlcNAc cycling influences α-synuclein amplification, degradation, and associated neuroinflammatory pathology.Molecular neurodegeneration · 2025Article
- Co-treatment Strategy Supports Neuroprotection by Intersecting p62-Keap1-NRF2 and Autophagy Signaling Pathways in the Cellular Model of Parkinson's Disease.Cellular and molecular neurobiology · 2025Article
- Peripheral nerve injury-induced remodeling of the tumor-associated macrophages promotes immune evasion in breast cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- OGT-Mediated O-GlcNAcylation of ATF2 Protects Against Sepsis-Associated Encephalopathy by Inhibiting Microglial Pyroptosis.Neuroscience bulletin · 2025Article
- Brain O-GlcNAcylation: Bridging physiological functions, disease mechanisms, and therapeutic applications.Molecular psychiatry · 2025Review
- Characterization and chemoproteomic profiling of protein O-GlcNAcylation in SOD1-G93A mouse model.Molecular medicine (Cambridge, Mass.) · 2025Article
- Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
This study aimed to elucidate the role of O-GlcNAc cycling in 6-hydroxydopamine (6-OHDA)-induced Parkinson's disease (PD)-like neurodegeneration and the underlying mechanisms. We observed dose-dependent downregulation of O-GlcNAcylation, accompanied by an increase in O-GlcNAcase following 6-OHDA treatment in both mouse brain and Neuro2a cells. Interestingly, elevating O-GlcNAcylation through glucosamine (GlcN) injection provided protection against PD pathogenesis induced by 6-OHDA. At the behavioral level, GlcN mitigated motor deficits induced by 6-OHDA, as determined using the pole, cylinder, and apomorphine rotation tests. Furthermore, GlcN attenuated 6-OHDA-induced neuroinflammation and mitochondrial dysfunction. Notably, augmented O-GlcNAcylation, achieved through O-GlcNAc transferase (OGT) overexpression in mouse brain, conferred protection against 6-OHDA-induced PD pathology, encompassing neuronal cell death, motor deficits, neuroinflammation, and mitochondrial dysfunction. These collective findings suggest that O-GlcNAcylation plays a crucial role in the normal functioning of dopamine neurons. Moreover, enhancing O-GlcNAcylation through genetic and pharmacological means could effectively ameliorate neurodegeneration and motor impairment in an animal model of PD. These results propose a potential strategy for safeguarding against the deterioration of dopamine neurons implicated in PD pathogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.