SynthesisDer Nervenarzt2018
[Tauopathies : From molecule to therapy].
Synthesis in Der Nervenarzt, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- A novel lncRNA FAM151B-DT regulates degradation of aggregation prone proteins.Molecular psychiatry · 2025Article
- Progressive Supranuclear Palsy Syndrome: An Overview.IBRO neuroscience reports · 2024Review
- [Neuroprotective treatment of tauopathies].Der Nervenarzt · 2021Review
- Evolving concepts in progressive supranuclear palsy and other 4-repeat tauopathies.Nature reviews. Neurology · 2021Review
- Therapeutic Application of rTMS in Atypical Parkinsonian Disorders.Behavioural neurology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe microtubule-associated tau protein is the defining denominator of a group of neurodegenerative diseases termed tauopathies.
objectiveProvide a timely state of the art review on recent scientific advances in the field of tauopathies. MATERIAL AND
methodsSystematic review of the literature from the past 10 years.
resultsTau proteins are increasingly being recognized as a highly variable protein, underlying and defining a spectrum of molecularly defined diseases, with a clinical spectrum ranging from dementia to hypokinetic movement disorders. Genetic variation at the tau locus can trigger disease or modify disease risk. Tau protein alterations can damage nerve cells and propagate pathologies through the brain. Thus, tau proteins may serve both as a serological and imaging biomarker. Tau proteins also provide a broad spectrum of rational therapeutic interventions to prevent disease progression. This knowledge has led to modern clinical trials.
conclusionThe field of tauopathies is in a state of dynamic and rapid progress, requiring close interdisciplinary collaboration.
Indexed as
Identifiers
30120488What 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.