ArticleJournal of Alzheimer's disease : JAD2026
Tau clearance reverses touch neuron dysfunction in both young and aged
Article in Journal of Alzheimer's disease : JAD, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed.
- Tunable tau expression in C. elegans neurons reveals that early-AD tau phosphorylation selectively impacts behavior and mitochondrial quality control.Neurobiology of disease · 2026Article
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Abstract
BackgroundAlzheimer's disease (AD) is an age-related dementia and presents a growing medical and economic burden. AD is classically diagnosed via the accumulation and aggregation of amyloid-β and tau. Potential and FDA-approved therapies designed to clear these aggregates at best delay rather than prevent disease, indicating that the root cause of AD lay upstream of aggregate formation. Tau protein's phosphorylation is critical for AD progression, and phosphorylation at Threonine 231 is thought to be an early disease-associated, "gatekeeper" event.ObjectivePreviously, we showed that genomic, single-copy insertion of phosphomimetic human tau (T231E) into
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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.