ArticleMolecular psychiatry2022
SIRT1 deficiency increases O-GlcNAcylation of tau, mediating synaptic tauopathy.
Article in Molecular psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- Axonopathy: mechanisms and potential therapeutic targets for neurodegenerative diseases.Translational neurodegeneration · 2026Review
- OGT-Mediated O-GlcNAcylation of ATF2 Protects Against Sepsis-Associated Encephalopathy by Inhibiting Microglial Pyroptosis.Neuroscience bulletin · 2025Article
- IRF1 ameliorates synaptic dysfunction through the modulation of O-GlcNAcylation on GluN1 subunit of NMDAR.Alzheimer's research & therapy · 2025Article
- SIRT1 prevents noise-induced hearing loss by enhancing cochlear mitochondrial function.Cell communication and signaling : CCS · 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
- Pathobiochemistry of Aging and Neurodegeneration: Deregulation of NAD+ Metabolism in Brain Cells.Biomolecules · 2024Review
- Glycosylation in aging and neurodegenerative diseases.Acta biochimica et biophysica Sinica · 2024Review
- Liuwei Dihuang formula ameliorates chronic stress-induced emotional and cognitive impairments in mice by elevating hippocampal O-GlcNAc modification.Frontiers in neuroscience · 2023Article
- O-GlcNAcylation regulates extracellular signal-regulated kinase (ERK) activation in Alzheimer's disease.Frontiers in aging neuroscience · 2023Article
- Phosphorylated Tau in Alzheimer's Disease and Other Tauopathies.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperphosphorylation of the microtubule associated protein tau is associated with several neurodegenerative diseases including Alzheimer's Disease (AD), collectively referred to as tauopathies. However, the mechanisms by which tau is linked to synaptic dysfunction and memory impairment remain unclear. To address this question, we constructed a mouse model with brain-specific deficiency of SIRT1 (SIRT1 flox/Cre + ). Here, we show that increase of site-specific phosphorylation of tau is coupled with the strengthened O-GlcNAcylation of tau triggered by reduced O-GlcNAcase (OGA) and increased O-GlcNAc transferase (OGT) protein level in the brain of SIRT1 flox/Cre+ mice. SIRT1 deletion in mice brain changes the synaptosomal distribution of site-specific phospho-tau. Learning and memory deficiency induced by dendritic spine deficits and synaptic dysfunction are revealed via SIRT1 flox/Cre+ mice. Our results provide evidence for SIRT1 as a potential therapeutic target in clinical tauopathies.
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