ArticleRegenerative therapy2025
Article in Regenerative therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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Who cites it
4 citing papers in PubMed.
- Fyn kinase: a key mechanistic regulator and therapeutic target in tauopathy and neurodegenerative diseases.Translational neurodegeneration · 2026Review
- Evaluating MAPT p.A152T as a risk factor for the 3R tauopathy Pick's disease.Brain communications · 2026Article
- Human iPSC-derived cerebral organoids reveal oxytocin-mediated protection against amyloid-β pathology.Regenerative therapy · 2025Article
- Tau aggregation induces cell death in iPSC-derived neurons.Aging brain · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Tau protein plays a pivotal role in the pathogenesis of Alzheimer's disease (AD) and in regulating neuronal excitability. Among tau-coding microtubule associated protein tau ( Methods: To investigate the effects of Results: In excitatory neuronal cultures, the A152T mutation was found to enhance spontaneous neuronal activity and the association of tau and Fyn. However, in inhibitory neuron-enriched cultures, the A152T mutation did not affect neuronal activity. Inhibition of NMDA receptors (NMDAR) and the reduction of tau protein levels decreased neuronal excitability in both A152T/A152T and healthy control (WT/WT) excitatory neurons. In addition, the A152T mutation increased the interaction between tau and Fyn. These findings suggest that the tau-Fyn interaction plays a critical role in regulating neuronal activity under physiological conditions, while the A152T mutation enhances neuronal activity by strengthening this endogenous interaction between tau and Fyn. In addition, transcriptomic analysis revealed structural changes specific to excitatory neurons with the A152T mutation. Common changes observed in both A152T and P301S lines recapitulated a dedifferentiation phenotype, consistent with previous reports. Conclusions: These data demonstrate that the A152T mutation in the
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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 Socratic graph.