ArticleNeuroscience2016
Tau pathology-mediated presynaptic dysfunction.
Article in Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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.
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Who cites it
42 citing papers in PubMed, 63 citations in OpenAlex.
- 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
- Inhibition of pathogenic tau signaling via blocking of the phosphatase-activating domain by novel small molecules.Frontiers in pharmacology · 2026Article
- Cytoskeletal Proteins and Alzheimer's Disease Pathogenesis: Focusing on the Interplay with Tau Pathology.Biomolecules · 2025Review
- Towards realistic simulation of disease progression in the visual cortex with CNNs.Scientific reports · 2025Article
- Distinct subcellular localization of tau and alpha-synuclein in lewy body disease.Acta neuropathologica communications · 2025Article
- Dysregulated calcium signaling in the aged primate association cortices: vulnerability to Alzheimer's disease neuropathology.Frontiers in aging neuroscience · 2025Review
- The PANoptosis-related hippocampal molecular subtypes and key biomarkers in Alzheimer's disease patients.Scientific reports · 2024Article
- Targeting synaptic pathology in Alzheimer's disease.Zoological research · 2024Article
- Tau, microtubule dynamics, and axonal transport: New paradigms for neurodegenerative disease.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023Article
- Amyloid β-based therapy for Alzheimer's disease: challenges, successes and future.Signal transduction and targeted therapy · 2023Review
- Deleterious and protective effects of epothilone-D alone and in the context of amyloid β- and tau-induced alterations.Frontiers in molecular neuroscience · 2023Article
- Alzheimer's disease as a synaptopathy: Evidence for dysfunction of synapses during disease progression.Frontiers in synaptic neuroscience · 2023Review
- Differential expression of tau species and the association with cognitive decline and synaptic loss in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Article
- The role of pathological tau in synaptic dysfunction in Alzheimer's diseases.Translational neurodegeneration · 2021Review
- Non-Canonical Roles of Tau and Their Contribution to Synaptic Dysfunction.International journal of molecular sciences · 2021Review
- Amyloid Prefibrillar Oligomers: The Surprising Commonalities in Their Structure and Activity.International journal of molecular sciences · 2021Review
- Tau Oligomers Neurotoxicity.Life (Basel, Switzerland) · 2021Review
- Increased neuronal activity in motor cortex reveals prominent calcium dyshomeostasis in tauopathy mice.Neurobiology of disease · 2021Article
- Tau: A Signaling Hub Protein.Frontiers in molecular neuroscience · 2021Article
- Differential compartmental processing and phosphorylation of pathogenic human tau and native mouse tau in the line 66 model of frontotemporal dementia.The Journal of biological chemistry · 2020Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
Brain tauopathies are characterized by abnormal processing of tau protein. While somatodendritic tau mislocalization has attracted considerable attention in tauopathies, the role of tau pathology in axonal transport, connectivity and related dysfunctions remains obscure. We have previously shown using the squid giant synapse that presynaptic microinjection of recombinant human tau protein (htau42) results in failure of synaptic transmission. Here, we evaluated molecular mechanisms mediating this effect. Thus, the initial event, observed after htau42 presynaptic injection, was an increase in transmitter release. This event was mediated by calcium release from intracellular stores and was followed by a reduction in evoked transmitter release. The effect of htau42 on synaptic transmission was recapitulated by a peptide comprising the phosphatase-activating domain of tau, suggesting activation of phosphotransferases. Accordingly, findings indicated that htau42-mediated toxicity involves the activities of both GSK3 and Cdk5 kinases.
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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.