Evidence map›Paper›PMID 37714405›Full record

ReviewDrug discovery today2023

TDP-43 protein interactome informs about perturbed canonical pathways and may help develop personalized medicine approaches for patients with TDP-43 pathology.

Benjamin R Helmold, Kate E Pauss, P Hande Ozdinler

Open access · hybridAbstract readReview
In one paragraph

Review in Drug discovery today, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

9 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. TDP-43: [GU]-ardian of the transcriptome.Molecular neurodegeneration · 2026
    Review
  4. Article
  5. Neurodegenerative spliceosomopathies.Frontiers in cell and developmental biology · 2026
    Review
  6. Article
  7. Article
  8. Context-dependent Interactors Regulate TDP-43 Dysfunction in ALS/FTLD.bioRxiv : the preprint server for biology · 2025
    Article
  9. Review
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

3 authors at 1 institution in 1 country.

Benjamin R HelmoldDepartment of Neurology, Feinberg School of Medicine, Northwestern University, 303 E. Chicago Ave, Chicago, IL, 60611, USA.
Kate E PaussDepartment of Neurology, Feinberg School of Medicine, Northwestern University, 303 E. Chicago Ave, Chicago, IL, 60611, USA.
P Hande OzdinlerDepartment of Neurology, Feinberg School of Medicine, Northwestern University, 303 E. Chicago Ave, Chicago, IL, 60611, USA; Center for Molecular Innovation and Drug Discovery, Center for Developmental Therapeutics, Chemistry of Life Processes Institute, Northwestern University, Evanston, IL 60611, USA; Mesulam Center for Cognitive Neurology and Alzheimer's Disease, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Feinberg School of Medicine, Les Turner ALS Center at Northwestern University, Chicago, IL 60611, USA. Electronic address: ozdinler@northwestern.edu.
Northwestern University · US

Funding

Novel Protein Aggregation Inhibitors and Upper Motor Neuron Stabilizers for ALS and other Neurodegenerative DiseasesR01AG061708 · NIA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI WILLIAM L KLEIN, Pembe Hande Ozdinler · 2019 to 2026
$10.5M
NIA NIH HHS R01 AG061708
6 · The paper itself

Abstract

Transactive response DNA binding protein of 43 kDa (TDP-43) pathology is a common proteinopathy observed among a broad spectrum of patients with neurodegenerative disease, regardless of the mutation. This suggests that protein-protein interactions of TDP-43 with other proteins may in part be responsible for the pathology. To gain better insights, we investigated TDP-43-binding proteins in each domain and correlated these interactions with canonical pathways. These investigations revealed key cellular events that are involved and are important at each domain and suggested previously identified compounds to modulate key aspects of these canonical pathways. Our approach proposes that personalized medicine approaches, which focus on perturbed cellular mechanisms would be feasible in the near future.

Indexed as

Amyotrophic Lateral SclerosisNeurodegenerative DiseasesTDP-43 ProteinopathiesDNA-Binding ProteinsHumansMutationPrecision MedicineDNA-Binding Proteinscanonical pathwayspersonalized medicineprecision medicineprotein–protein interactionsTDP-43

Identifiers

PMID37714405
PMCPMC10872580
OpenAlexW4386700922

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.