Evidence map›Paper›PMID 36555399›Full record

ReviewInternational journal of molecular sciences2022

TDP-43 Proteinopathy and Tauopathy: Do They Have Pathomechanistic Links?

Yuichi Riku, Mari Yoshida, Yasushi Iwasaki, Gen Sobue, Masahisa Katsuno, Shinsuke Ishigaki

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

21 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Atypical features including acquired oculomotor apraxia inJournal of neuromuscular diseases · 2026
    Article
  3. Review
  4. Review
  5. Primary age-related tauopathy.Acta neuropathologica · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Inducers and modulators of protein aggregation in Alzheimer's disease - Critical tools for understanding the foundations of aggregate structures.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. A framework for translating tauopathy therapeutics: Drug discovery to clinical trials.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Review
  15. Article
  16. Article
  17. Review
  18. Targeting Progranulin as an Immuno-Neurology Therapeutic Approach.International journal of molecular sciences · 2023
    Review
  19. Review
  20. Article
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

6 authors.

Yuichi RikuInstitute for Medical Science of Aging, Aichi Medical University, Nagakute 480-1195, Japan.ORCID 0000-0002-6493-8976
Mari YoshidaInstitute for Medical Science of Aging, Aichi Medical University, Nagakute 480-1195, Japan.
Yasushi IwasakiInstitute for Medical Science of Aging, Aichi Medical University, Nagakute 480-1195, Japan.ORCID 0000-0002-0059-3104
Gen SobueGraduate School of Medicine, Aichi Medical University, Nagakute 480-1195, Japan.
Masahisa KatsunoDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya 744-8550, Japan.ORCID 0000-0001-9453-9311
Shinsuke IshigakiMolecular Neuroscience Research Center, Shiga University of Medical Science, Otsu 520-2192, Japan.

Funding

AMED JP20ek0109392 (M.Y.), JP20ek0109391 (M.Y.), 21dm0207116 (S.I.), and 21ek0109497 (S.I.)Grants-in-Aid from the Research Committee of CNS Degenerative Diseases, Research on Policy Planning and Evaluation for Rare and Intractable Diseases, Health, Labour, and Welfare Sciences Research Grants, the Ministry of Health, Labour, and Welfare no number applicable (Y.I.)Intramural Research Grant for Neurological and Psychiatric Disorders of NCNP 30-8 (M.Y.)JSPS KAKENHI JP20K16586 (Y.R.) and 21H02838 (S.I.)
6 · The paper itself

Abstract

Transactivation response DNA binding protein 43 kDa (TDP-43) and tau are major pathological proteins of neurodegenerative disorders, of which neuronal and glial aggregates are pathological hallmarks. Interestingly, accumulating evidence from neuropathological studies has shown that comorbid TDP-43 pathology is observed in a subset of patients with tauopathies, and vice versa. The concomitant pathology often spreads in a disease-specific manner and has morphological characteristics in each primary disorder. The findings from translational studies have suggested that comorbid TDP-43 or tau pathology has clinical impacts and that the comorbid pathology is not a bystander, but a part of the disease process. Shared genetic risk factors or molecular abnormalities between TDP-43 proteinopathies and tauopathies, and direct interactions between TDP-43 and tau aggregates, have been reported. Further investigations to clarify the pathogenetic factors that are shared by a broad spectrum of neurodegenerative disorders will establish key therapeutic targets.

Indexed as

Frontotemporal Lobar DegenerationNeurodegenerative DiseasesTauopathiesTDP-43 ProteinopathiesDNA-Binding ProteinsHumanstau ProteinsDNA-Binding Proteinstau ProteinsADALSCBDFTLDLATEPARTPSPSFPQtauTDP-43

Identifiers

PMID36555399
PMCPMC9779029

What OpenQuestion holds

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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 OpenQuestion graph.