ArticleeLife2016
Tau and spectraplakins promote synapse formation and maintenance through Jun kinase and neuronal trafficking.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Similarities and Differences in the Pattern of Tau Hyperphosphorylation in Physiological and Pathological Conditions: Impacts on the Elaboration of Therapies to Prevent Tau Pathology.Frontiers in neurology · 2020Pooled it
- Aging-associated modulation of UFMylation impairs proteostasis in C. elegans.Nature communications · 2026Article
- GSK-3β coordinates axonal microtubule organization through Shot and Tau.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Soma-localized Rab39 inhibits synaptic autophagy by controlling trafficking of Atg9 vesicles.The EMBO journal · 2025Article
- Glucose uptake in pigment glia suppresses Tau-induced inflammation and photoreceptor degeneration.Disease models & mechanisms · 2025Article
- Oxidative Stress Promotes Axonal Atrophy through Alterations in Microtubules and EB1 Function.Aging and disease · 2024Article
- Neuronal ageing is promoted by the decay of the microtubule cytoskeleton.PLoS biology · 2024Article
- Puckered and JNK signaling in pioneer neurons coordinates the motor activity of the Drosophila embryo.Nature communications · 2023Article
- Alzheimer's disease: an axonal injury disease?Frontiers in aging 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
- FTD-associated mutations in Tau result in a combination of dominant and recessive phenotypes.Neurobiology of disease · 2022Article
- Drosophila Primary Neuronal Cultures as a Useful Cellular Model to Study and Image Axonal Transport.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Tau Acts in Concert With Kinase/Phosphatase Underlying Synaptic Dysfunction.Frontiers in aging neuroscience · 2022Review
- Cytoskeleton and Associated Proteins: Pleiotropic JNK Substrates and Regulators.International journal of molecular sciences · 2021Review
- Association of neurogranin gene expression with Alzheimer's disease pathology in the perirhinal cortex.Alzheimer's & dementia (New York, N. Y.) · 2021Article
- Article
- Defined Tau Phosphospecies Differentially Inhibit Fast Axonal Transport Through Activation of Two Independent Signaling Pathways.Frontiers in molecular neuroscience · 2020Article
- Article
- The model of local axon homeostasis - explaining the role and regulation of microtubule bundles in axon maintenance and pathology.Neural development · 2019Review
- Synaptic distributions of pS214-tau in rhesus monkey prefrontal cortex are associated with spine density, but not with cognitive decline.The Journal of comparative neurology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The mechanisms regulating synapse numbers during development and ageing are essential for normal brain function and closely linked to brain disorders including dementias. Using Drosophila, we demonstrate roles of the microtubule-associated protein Tau in regulating synapse numbers, thus unravelling an important cellular requirement of normal Tau. In this context, we find that Tau displays a strong functional overlap with microtubule-binding spectraplakins, establishing new links between two different neurodegenerative factors. Tau and the spectraplakin Short Stop act upstream of a three-step regulatory cascade ensuring adequate delivery of synaptic proteins. This cascade involves microtubule stability as the initial trigger, JNK signalling as the central mediator, and kinesin-3 mediated axonal transport as the key effector. This cascade acts during development (synapse formation) and ageing (synapse maintenance) alike. Therefore, our findings suggest novel explanations for intellectual disability in Tau deficient individuals, as well as early synapse loss in dementias including Alzheimer's disease.
Indexed as
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.