Evidence map›Paper›PMID 42401929›Full record

ArticleMolecular neurodegeneration2026

TDP-43 dysfunction facilitates the pathological conversion of tau.

Meghraj S Baghel, Grace D Burns, Margarita Tsapatsis, Aswathy Peethambaran Mallika, Anna Lourdes F Cruz, Tianyu Cao, Xiaoke K Chen, Isabel De La Rosa, Shaelyn R Marx, Yingzhi Ye and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular neurodegeneration, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Meghraj S Baghel *Department of Pathology, The Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Grace D Burns *Department of Pathology, The Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Margarita TsapatsisDepartment of Pathology, The Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Aswathy Peethambaran MallikaDepartment of Pathology, The Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Anna Lourdes F CruzDepartment of Pathology, The Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Tianyu CaoDepartment of Pathology, The Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Xiaoke K ChenDepartment of Pathology, The Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Isabel De La RosaDepartment of Pathology, The Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Shaelyn R MarxDepartment of Pathology, The Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Yingzhi YeDepartment of Physiology, The Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Shuying SunDepartment of Pathology, The Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Tong LiDepartment of Pathology, The Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Jonathan P LingDepartment of Pathology, The Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Philip C WongDepartment of Pathology, The Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, 21205, USA. wong@jhmi.edu.

Funding

TDP-43 Proteinopathy in ALS-FTD: Mechanism, Target Validation and BiomarkerR01NS095969 · NINDS · JOHNS HOPKINS UNIVERSITY · PI PHILIP C WONG · 2016 to 2026
$2.4M
Generation and characterization of a mouse model exhibiting beta-amyloidosis and tauopathy with nuclear depletion of TDP-43R61NS115161 · NINDS · JOHNS HOPKINS UNIVERSITY · PI WONG, PHILIP C · 2019 to 2019
$2.2M
Generation and characterization of a mouse model exhibiting beta-amyloidosis and tauopathy with nuclear depletion of TDP-43R33NS115161 · NINDS · JOHNS HOPKINS UNIVERSITY · PI WONG, PHILIP C · 2022 to 2023
$1.3M
NINDS NIH HHS R01 NS095969NINDS NIH HHS R33 NS115161NINDS NIH HHS R61 NS115161
6 · The paper itself

Abstract

TDP-43 proteinopathy coexists with tauopathy in a variety of neurodegenerative disorders, including Alzheimer's Disease (AD) and AD related dementia (ADRD). While such co-pathology of TDP-43 is strongly associated with worsened neurodegeneration, the pathogenic mechanism underlying the exacerbated neuron loss remains elusive. Loss of TDP-43 splicing repression occurring during the early stage of neurodegenerative disease suggests that such loss could facilitate the pathological conversion of tau. Here, we report that TDP-43 loss-of-function (LOF) in forebrain neurons (Tau4R; CaMKII-CreER; Tardbp

Indexed as

DNA-Binding ProteinsTauopathiestau ProteinsTDP-43 ProteinopathiesAlzheimer DiseaseAnimalsBrainDisease Models, AnimalHumansMiceMice, TransgenicNeuronsDNA-Binding ProteinsTARDBP protein, humantau ProteinsADRDAlzheimer’s diseaseCaspaseCo-pathologyFTDMouse modelNeurodegenerationTauTauopathyTDP-43Vulnerable neuron

Identifiers

PMID42401929
PMCPMC13613616

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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.