Evidence map›Paper›PMID 37849894›Full record

ArticleFrontiers in neuroscience2023

Loss of TDP-43 function contributes to genomic instability in amyotrophic lateral sclerosis.

Minggang Fang, Sara K Deibler, Alissa L Nana, Sarat C Vatsavayai, Shahid Banday, You Zhou, Sandra Almeida, Alexandra Weiss, Robert H Brown, William W Seeley and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 3 pooled it
2.5field-weighted citation impact, top 10% 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

14 citing papers in PubMed, 3 syntheses or guidelines pooled it, 12 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. TDP-43: [GU]-ardian of the transcriptome.Molecular neurodegeneration · 2026
    Review
  5. Article
  6. Article
  7. ALS and Huntington Disease: Unraveling the Connections between TDP-43 and Huntingtin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. 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

12 authors at 3 institutions in 1 country.

Minggang FangDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Chan Medical School, Worcester, MA, United States.
Sara K DeiblerDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Chan Medical School, Worcester, MA, United States.
Alissa L NanaDepartment of Neurology, Memory and Aging Center, University of California, San Francisco, San Francisco, CA, United States.
Sarat C VatsavayaiDepartment of Neurology, Memory and Aging Center, University of California, San Francisco, San Francisco, CA, United States.
Shahid BandayDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Chan Medical School, Worcester, MA, United States.
You ZhouDepartment of Neurology, University of Massachusetts Chan Medical School, Worcester, MA, United States.
Sandra AlmeidaDepartment of Neurology, University of Massachusetts Chan Medical School, Worcester, MA, United States.
Alexandra WeissDepartment of Neurology, University of Massachusetts Chan Medical School, Worcester, MA, United States.
Robert H BrownDepartment of Neurology, University of Massachusetts Chan Medical School, Worcester, MA, United States.
William W SeeleyDepartment of Neurology, Memory and Aging Center, University of California, San Francisco, San Francisco, CA, United States.
Fen-Biao GaoDepartment of Neurology, University of Massachusetts Chan Medical School, Worcester, MA, United States.
Michael R GreenDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Chan Medical School, Worcester, MA, United States.
University of Massachusetts Chan Medical School · USUniversity of California, San Francisco · USUniversity Memory and Aging Center · US

Funding

Technology and Remote Assessment CoreU19AG063911 · NIA · MAYO CLINIC ROCHESTER · PI ADAM L. BOXER, Bradley F Boeve · 2019 to 2026
$120.9M
Early Onset AD Consortium - the LEAD Study (LEADS)U01AG057195 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI APOSTOLOVA, LIANA G, CARRILLO, MARIA C · 2018 to 2023
$70.3M
TDP-43 Loss-of-Function: Biology to BiomarkersP01AG019724 · NIA · UNIVERSITY OF PENNSYLVANIA · PI Jennifer Merrilees · 2002 to 2026
$67.2M
Research Education ComponentP30AG062422 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Serggio Carlo Lanata · 2019 to 2026
$36.9M
SPLICING OF MRNA PRECURSORSR01GM035490 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI GREEN, MICHAEL R · 1985 to 2021
$4.7M
Deep Pathological Phenotyping in Frontotemporal Dementia and Motor Neuron Disease.R01NS104437 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SEELEY, WILLIAM W · 2018 to 2022
$4.3M
Investigating Pathogenic Mechanisms of Frontotemporal Dementia Caused by Mutations in CHMP2B and TBK1R37NS057553 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI GAO, FEN-BIAO · 2018 to 2024
$4.3M
Understanding Frontotemporal Dementia Using Drosophila and iPSC ModelsR01NS101986 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI Fen-Biao Gao · 2017 to 2026
$3.6M
Understanding Frontotemporal Dementia Using Drosophila and iPSC ModelsRF1NS101986 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI GAO, FEN-BIAO · 2022 to 2022
$2.1M
Characterization of TASK-1 Modulation of Dipeptide Repeat Protein-Mediated Toxicity in iPSC-derived C9ORF72 Patient Neurons.R21NS119952 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI ALMEIDA, SANDRA · 2020 to 2020
$461k
Investigating Translational De-repression as a Mechanism to Increase Progranulin Levels in iPSC-derived Patient NeuronsR21NS112766 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI ALMEIDA, SANDRA · 2019 to 2019
$461k
NIA NIH HHS P01 AG019724NIA NIH HHS P30 AG062422NIA NIH HHS U01 AG057195NIA NIH HHS U19 AG063911NIGMS NIH HHS R01 GM035490NINDS NIH HHS R01 NS101986NINDS NIH HHS R01 NS104437NINDS NIH HHS R21 NS112766NINDS NIH HHS R21 NS119952NINDS NIH HHS R37 NS057553NINDS NIH HHS RF1 NS101986
6 · The paper itself

Abstract

A common pathological hallmark of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is the cytoplasmic mislocalization and aggregation of the DNA/RNA-binding protein TDP-43, but how loss of nuclear TDP-43 function contributes to ALS and FTD pathogenesis remains largely unknown. Here, using large-scale RNAi screening, we identify

Indexed as

amyotrophic lateral sclerosisDNA repairfrontotemporal dementiagenomic instabilityhomologous recombinationTDP-43

Identifiers

PMID37849894
PMCPMC10577185
OpenAlexW4387266489

What OpenQuestion 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 OpenQuestion graph.