Evidence map›Paper›PMID 35392986›Full record

ReviewMolecular neurodegeneration2022

Tauopathies: new perspectives and challenges.

Yi Zhang, Kai-Min Wu, Liu Yang, Qiang Dong, Jin-Tai Yu

Open access · goldAbstract readReview
In one paragraph

Review in Molecular neurodegeneration, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 184 papers.

0numbers the graph read from it
0cells of the map it votes in
184citing papers in PubMed
32.4field-weighted citation impact, top 1% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

184 citing papers in PubMed, 282 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Neuroinflammation and Tauopathies.Molecular biology reports · 2026
    Review
  11. Impact of reducedEJNMMI physics · 2026
    Article
  12. Riboregulation: a non-canonical tau function.Molecular neurodegeneration · 2026
    Review
  13. Article
  14. Article
  15. Brain regional susceptibility to tauopathy in individuals at risk for chronic traumatic encephalopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article

124 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Yi ZhangDepartment of Neurology and Institute of Neurology, Huashan Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, National Center for Neurological Disorders, 12th Wulumuqi Zhong Road, Shanghai, 200040, China.
Kai-Min WuDepartment of Neurology and Institute of Neurology, Huashan Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, National Center for Neurological Disorders, 12th Wulumuqi Zhong Road, Shanghai, 200040, China.
Liu YangDepartment of Neurology and Institute of Neurology, Huashan Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, National Center for Neurological Disorders, 12th Wulumuqi Zhong Road, Shanghai, 200040, China.
Qiang DongDepartment of Neurology and Institute of Neurology, Huashan Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, National Center for Neurological Disorders, 12th Wulumuqi Zhong Road, Shanghai, 200040, China.
Jin-Tai YuDepartment of Neurology and Institute of Neurology, Huashan Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, National Center for Neurological Disorders, 12th Wulumuqi Zhong Road, Shanghai, 200040, China. jintai_yu@fudan.edu.cn.ORCID 0000-0002-7686-0547
Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTauopathies are a class of neurodegenerative disorders characterized by neuronal and/or glial tau-positive inclusions. MAIN BODY: Clinically, tauopathies can present with a range of phenotypes that include cognitive/behavioral-disorders, movement disorders, language disorders and non-specific amnestic symptoms in advanced age. Pathologically, tauopathies can be classified based on the predominant tau isoforms that are present in the inclusion bodies (i.e., 3R, 4R or equal 3R:4R ratio). Imaging, cerebrospinal fluid (CSF) and blood-based tau biomarkers have the potential to be used as a routine diagnostic strategy and in the evaluation of patients with tauopathies. As tauopathies are strongly linked neuropathologically and genetically to tau protein abnormalities, there is a growing interest in pursuing of tau-directed therapeutics for the disorders. Here we synthesize emerging lessons on tauopathies from clinical, pathological, genetic, and experimental studies toward a unified concept of these disorders that may accelerate the therapeutics.

conclusionsSince tauopathies are still untreatable diseases, efforts have been made to depict clinical and pathological characteristics, identify biomarkers, elucidate underlying pathogenesis to achieve early diagnosis and develop disease-modifying therapies.

Indexed as

Neurodegenerative DiseasesTauopathiesHumansInclusion BodiesNeuronsProtein Isoformstau ProteinsProtein Isoformstau ProteinsBiomarkersGeneticsNeurodegenerationTauopathiesTherapeutics

Identifiers

PMID35392986
PMCPMC8991707
OpenAlexW4223629343

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.