ArticleProceedings of the National Academy of Sciences of the United States of America2020
Sulfhydration of AKT triggers Tau-phosphorylation by activating glycogen synthase kinase 3β in Alzheimer's disease.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 36 papers.
What it found
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Who cites it
36 citing papers in PubMed, 64 citations in OpenAlex.
- The Effect of Rivastigmine on Enhanced Glucose Metabolism and Enhanced Synaptic Plasticity in the Hippocampus of Aged Rats: A Sex-Dependent Study.International journal of molecular sciences · 2026Article
- Hydrogen sulfide-mediated protein s-persulfidation: a regulatory mechanism in cardiovascular homeostasis.Molecular medicine (Cambridge, Mass.) · 2026Review
- The insulin receptor inhibitor BMS-754807 alleviates neuroinflammation and Alzheimer's disease pathologies across human cellular and mouse models.Journal of neuroinflammation · 2026Article
- PROTAC-mediated multi-target protein degradation in Alzheimer's disease: mechanistic insights, therapeutic applications, and translational challenges.RSC medicinal chemistry · 2026Review
- HIV and Cocaine exposure promote Tau phosphorylation through RSK-1 in a GSK3β-independent manner.bioRxiv : the preprint server for biology · 2026Article
- S-sulfhydration: Novel insights into the antioxidant and antiinflammation in age-related diseases.Journal of advanced research · 2026Review
- Glycyrrhizic Acid Attenuates AβCells · 2026Article
- Neuroprotective mechanism of hydrogen sulfide in okadaic acid-induced alzheimer-like pathology.GeroScience · 2026Article
- Engineering exosomes for targeted neurodegenerative therapy: innovations in biogenesis, drug loading, and clinical translation.Theranostics · 2026Review
- Neuroinflammation in Alzheimer's disease: glial crosstalk, pathological modulation, and therapeutic implications.Frontiers in immunology · 2026Review
- [Mediation analysis of plasma phosphorylated tau217 in the association between periodontitis and mild cognitive impairment].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2025Article
- Microglia aggregates define distinct immune and neurodegenerative niches in Alzheimer's disease hippocampus.Acta neuropathologica · 2025Article
- Essential role of sulfide oxidation in brain health and neurological disorders.Pharmacology & therapeutics · 2025Review
- Cerebral endothelial 3-mercaptopyruvate sulfurtransferase improves ischemia-induced cognitive impairmentActa pharmaceutica Sinica. B · 2025Article
- Depression like-behavior and memory loss induced by methylglyoxal is associated with tryptophan depletion and oxidative stress: a new in vivo model of neurodegeneration.Biological research · 2024Article
- Oxidative Cysteine Post Translational Modifications Drive the Redox Code Underlying Neurodegeneration and Amyotrophic Lateral Sclerosis.Antioxidants (Basel, Switzerland) · 2024Review
- GSK3: A potential target and pending issues for treatment of Alzheimer's disease.CNS neuroscience & therapeutics · 2024Review
- Mouse serum albumin induces neuronal apoptosis and tauopathies.Acta neuropathologica communications · 2024Article
- P25/CDK5-mediated Tau Hyperphosphorylation in Both Ipsilateral and Contralateral Cerebra Contributes to Cognitive Deficits in Post-stroke Mice.Current medical science · 2023Article
- Tau and neuroinflammation in Alzheimer's disease: interplay mechanisms and clinical translation.Journal of neuroinflammation · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
In Alzheimer's disease (AD), human Tau is phosphorylated at S199 (hTau-S199-P) by the protein kinase glycogen synthase kinase 3β (GSK3β). HTau-S199-P mislocalizes to dendritic spines, which induces synaptic dysfunction at the early stage of AD. The AKT kinase, once phosphorylated, inhibits GSK3β by phosphorylating it at S9. In AD patients, the abundance of phosphorylated AKT with active GSK3β implies that phosphorylated AKT was unable to inactivate GSK3β. However, the underlying mechanism of the inability of phosphorylated AKT to phosphorylate GSK3β remains unknown. Here, we show that total AKT and phosphorylated AKT was sulfhydrated at C77 due to the induction of intracellular hydrogen sulfide (H
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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.