ArticleProceedings of the National Academy of Sciences of the United States of America2016
Loss of O-GlcNAc glycosylation in forebrain excitatory neurons induces neurodegeneration.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers.
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Who cites it
129 citing papers in PubMed, 223 citations in OpenAlex.
- Timing and duration of diabetes and incident dementia in older adults: a prospective cohort study.Alzheimer's research & therapy · 2026Article
- Chemical biology tools for the O-GlcNAc modification: Determining systems-level functions and druggability.Current opinion in chemical biology · 2026Review
- 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
- Functional analysis of O-GlcNAcylation by networking of OGT interactors and substrates.Nature chemical biology · 2026Article
- Mechanoresponsive modulation of nuclear pore complex structure and function bybioRxiv : the preprint server for biology · 2026Article
- The Effect of Metabolic Syndrome on Alzheimer's Disease: Physical Activity as a Preventive and Therapeutic Measure.Brain sciences · 2026Review
- The Hsp40 cochaperone DNAJC7 regulates polyglutamine aggregation and exhibits context-dependent effects on polyglycine aggregation.The Journal of biological chemistry · 2026Article
- GalNAc-T13 maintains neurite architecture and memory retention via O-GalNAc glycosylation of seizure protein 6.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Pharmacological inhibition of O-GlcNAcase reduces pS129-α-synuclein positive aggregates in the substantia nigra of mThy1-hSNCA mice.Journal of Parkinson's disease · 2026Article
- O-GlcNAcylation at the tumor-immune interface: a metabolic post-translational code driving immune evasion and therapy resistance in cancer.Frontiers in immunology · 2026Review
- Breaking the proteasome balance: α-synuclein and the ubiquitin-proteasome system.Frontiers in cell and developmental biology · 2026Review
- Targeting O-GlcNAcylation: Novel Therapeutic Strategies for Neurological Disease.Molecular neurobiology · 2025Review
- Unlocking the Sugar Code: Implications and Consequences of Glycosylation in Alzheimer's Disease and Other Tauopathies.Biomedicines · 2025Review
- Unlocking extracellular mitochondria from bench to clinical application in stroke.Stem cells translational medicine · 2025Review
- Zscan4 as a Candidate Conveyor of Early Developmental Defects in O-GlcNAc Transferase Intellectual Disability.Molecular & cellular proteomics : MCP · 2025Article
- Modulation of O-GlcNAc cycling influences α-synuclein amplification, degradation, and associated neuroinflammatory pathology.Molecular neurodegeneration · 2025Article
- IRF1 ameliorates synaptic dysfunction through the modulation of O-GlcNAcylation on GluN1 subunit of NMDAR.Alzheimer's research & therapy · 2025Article
- O-GlcNAc modulation of nuclear pore complexes orchestrates mRNA export efficiency.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Brain O-GlcNAcylation: Bridging physiological functions, disease mechanisms, and therapeutic applications.Molecular psychiatry · 2025Review
69 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
O-GlcNAc glycosylation (or O-GlcNAcylation) is a dynamic, inducible posttranslational modification found on proteins associated with neurodegenerative diseases such as α-synuclein, amyloid precursor protein, and tau. Deletion of the O-GlcNAc transferase (ogt) gene responsible for the modification causes early postnatal lethality in mice, complicating efforts to study O-GlcNAcylation in mature neurons and to understand its roles in disease. Here, we report that forebrain-specific loss of OGT in adult mice leads to progressive neurodegeneration, including widespread neuronal cell death, neuroinflammation, increased production of hyperphosphorylated tau and amyloidogenic Aβ-peptides, and memory deficits. Furthermore, we show that human cortical brain tissue from Alzheimer's disease patients has significantly reduced levels of OGT protein expression compared with cortical tissue from control individuals. Together, these studies indicate that O-GlcNAcylation regulates pathways critical for the maintenance of neuronal health and suggest that dysfunctional O-GlcNAc signaling may be an important contributor to neurodegenerative diseases.
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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.