ArticleNature communications2017
Tau association with synaptic vesicles causes presynaptic dysfunction.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 253 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
253 citing papers in PubMed, 2 syntheses or guidelines pooled it, 441 citations in OpenAlex.
- A Meta-Analysis on Presynaptic Changes in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2024Pooled it
- Deregulated mitochondrial microRNAs in Alzheimer's disease: Focus on synapse and mitochondria.Ageing research reviews · 2022Pooled it
- A phase 2 double-blind placebo-controlled 24-week treatment clinical study of the p38 alpha kinase inhibitor neflamapimod in mild Alzheimer's disease.Alzheimer's research & therapy · 2021Trial
- Elevation of the mechanically-sensitive e protein emerin links nuclear mechanotransduction to tau-induced cytoskeletal remodeling in neurons.Nucleus (Austin, Tex.) · 2026Article
- Widespread synaptic density loss in schizophrenia follows molecular and network architecture.Molecular psychiatry · 2026Article
- Temporal Trajectories of the Tau Aggregate Interactome Reveal Stage-Specific Vulnerabilities in Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Quantitative Analysis of Axonal Degeneration and TDP-43 Aggregation in Compartmentalized Human iPSC-Derived Motor Neuron-Myotube Co-cultures.Bio-protocol · 2026Article
- Tau Disaggregation by a CNS-Permeable Small Molecule Reduces Fibril and Oligomer Burden and Preserves Proteostasis and Behavior.bioRxiv : the preprint server for biology · 2026Article
- Review
- Article
- Tau-mediated Mechanisms in Alzheimer's Disease Pathogenesis.Molecular neurobiology · 2026Review
- Tau seeds induce neurofibrillary tangle formation across brain regions via individual-specific connectivity.Neuron · 2026Article
- Structures and Dynamics of Tau Assemblies from Solid-State NMR.Accounts of chemical research · 2026Article
- Distinct regional patterns of synaptic vulnerability across hippocampal and parahippocampal subregions in Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2026Article
- Omega-3 Fatty Acids and Alzheimer's Disease: Toward a New Understanding of Neuroprotective Mechanisms and Intervention Strategies.Marine drugs · 2026Review
- IgLON5 autoimmune antibodies activate Tau via neuronal hyperactivity.Science advances · 2026Article
- Longitudinal CSF and Serum Biomarker Dynamics in Tofersen-TreatedInternational journal of molecular sciences · 2026Article
- Spatial Single-Cell Proteomics Reveals Molecular Trajectories Of Tangle-Bearing Neurons In Alzheimer's Disease.bioRxiv : the preprint server for biology · 2026Article
- Diagnostic and prognostic utility of serum β-synuclein in Alzheimer's disease: a longitudinal cohort study.The journal of prevention of Alzheimer's disease · 2026Article
- Beyond microtubule regulation: the multifaceted roles of tau in neuronal function and dysfunction.Translational psychiatry · 2026Review
193 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 4 institutions in 3 countries.
Funding
Abstract
Tau is implicated in more than 20 neurodegenerative diseases, including Alzheimer's disease. Under pathological conditions, Tau dissociates from axonal microtubules and missorts to pre- and postsynaptic terminals. Patients suffer from early synaptic dysfunction prior to Tau aggregate formation, but the underlying mechanism is unclear. Here we show that pathogenic Tau binds to synaptic vesicles via its N-terminal domain and interferes with presynaptic functions, including synaptic vesicle mobility and release rate, lowering neurotransmission in fly and rat neurons. Pathological Tau mutants lacking the vesicle binding domain still localize to the presynaptic compartment but do not impair synaptic function in fly neurons. Moreover, an exogenously applied membrane-permeable peptide that competes for Tau-vesicle binding suppresses Tau-induced synaptic toxicity in rat neurons. Our work uncovers a presynaptic role of Tau that may be part of the early pathology in various Tauopathies and could be exploited therapeutically.
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Identifiers
What OpenQuestion holds
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.