ReviewJournal of neurochemistry2025
Limitations and Applications of Rodent Models in Tauopathy and Synucleinopathy Research.
Review in Journal of neurochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- Brainstem pathology in anti-IgLON5 disease: new insights into early events and tau progression.Brain : a journal of neurology · 2026Article
- Co-infection with two α-synuclein strains reveals novel synergistic interactions.Acta neuropathologica · 2025Article
- Co-infection with two α-synuclein strains reveals novel synergistic interactions.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Rodent models that accurately recapitulate key aspects of human disease have long been fundamental to the successful development of clinical interventions. This is greatly underscored in the neurodegenerative disease field, where preclinical testing of anti-prion therapeutics against rodent-adapted prions resulted in the development of small molecules effective against rodent-adapted prions but not against human prions. These findings provided critical lessons for ongoing efforts to develop treatments for patients with neurodegenerative diseases caused by misfolding and accumulation of the proteins tau and α-synuclein, or tauopathies and synucleinopathies, respectively. To avoid the potential pitfalls previously identified in the prion field, this review focuses on rodent models currently available to study tau and α-synuclein disease pathogenesis, emphasizing the strengths and limitations of each with the particular goal of better supporting preclinical research.
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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.