ReviewNeuromolecular medicine2020
O-GlcNAcylation as a Therapeutic Target for Alzheimer's Disease.
Review in Neuromolecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed.
- Enzymatic glycosylation as a potential molecular link between Alzheimer's disease and glaucoma.International journal of ophthalmology · 2026Review
- Involvement of uridine in brain and gut health: insights into its neuroprotective potential via the gut-brain axis.Pharmacological reports : PR · 2025Review
- Targeting O-GlcNAcylation: Novel Therapeutic Strategies for Neurological Disease.Molecular neurobiology · 2025Review
- Cross-Talk Between Tau O-GlcNAcylation and the Formation of the Early Driver of Neurodegeneration (Cis P-Thr231-Pro Tau) in Primary Cortical Neurons.Molecular neurobiology · 2025Article
- Unlocking extracellular mitochondria from bench to clinical application in stroke.Stem cells translational medicine · 2025Review
- OGT-Mediated O-GlcNAcylation of ATF2 Protects Against Sepsis-Associated Encephalopathy by Inhibiting Microglial Pyroptosis.Neuroscience bulletin · 2025Article
- Methylome analysis of FTLD patients with TDP-43 pathology identifies epigenetic signatures specific to pathological subtypes.Molecular neurodegeneration · 2025Article
- Recent Progress of Small-molecule Inhibitors of O-GlcNAcase for Alzheimer's Disease.Mini reviews in medicinal chemistry · 2025Review
- New progress on the role and mechanism of tau protein in Alzheimer's disease and depression.Frontiers in neurology · 2025Review
- Neural stem cells in adult neurogenesis and their therapeutic applications in neurodegenerative disorders: a concise review.Frontiers in molecular medicine · 2025Review
- Recent advances in potential enzymes and their therapeutic inhibitors for the treatment of Alzheimer's disease.Heliyon · 2024Review
- Astragalus polysaccharide treatment relieves cerebral ischemia‒reperfusion injury by promoting M2 polarization of microglia by enhancing O-GlcNAcylation.Metabolic brain disease · 2024Article
- TGF‑β/Smad signaling in chronic kidney disease: Exploring post‑translational regulatory perspectives (Review).Molecular medicine reports · 2024Review
- CanPharmaceuticals (Basel, Switzerland) · 2024Review
- O-GlcNAcylation: roles and potential therapeutic target for bone pathophysiology.Cell communication and signaling : CCS · 2024Review
- The Role of Oxygen Homeostasis and the HIF-1 Factor in the Development of Neurodegeneration.International journal of molecular sciences · 2024Review
- Phosphorylation and O-GlcNAcylation at the same α-synuclein site generate distinct fibril structures.Nature communications · 2024Article
- Involvement of Glucosamine 6 Phosphate Isomerase 2 (GNPDA2) Overproduction in β-Amyloid- and Tau P301L-Driven Pathomechanisms.Biomolecules · 2024Article
- The alteration and role of glycoconjugates in Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most common cause of dementia and the number of elderly patients suffering from AD has been steadily increasing. Despite worldwide efforts to cope with this disease, little progress has been achieved with regard to identification of effective therapeutics. Thus, active research focusing on identification of new therapeutic targets of AD is ongoing. Among the new targets, post-translational modifications which modify the properties of mature proteins have gained attention. O-GlcNAcylation, a type of PTM that attaches O-linked β-N-acetylglucosamine (O-GlcNAc) to a protein, is being sought as a new target to treat AD pathologies. O-GlcNAcylation has been known to modify the two important components of AD pathological hallmarks, amyloid precursor protein, and tau protein. In addition, elevating O-GlcNAcylation levels in AD animal models has been shown to be effective in alleviating AD-associated pathology. Although studies investigating the precise mechanism of reversal of AD pathologies by targeting O-GlcNAcylation are not yet complete, it is clearly important to examine O-GlcNAcylation regulation as a target of AD therapeutics. This review highlights the mechanisms of O-GlcNAcylation and its role as a potential therapeutic target under physiological and pathological AD conditions.
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Registered trials
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