Evidence map›Paper›PMID 41542616›Full record

ArticlebioRxiv : the preprint server for biology2026

Identification of molecular and clinical ALS subgroups based on TDP-43 loss of function molecular markers from population-based patient-derived iPS motor neurons.

Trinity Cheng, Shaili Tripathi, Yike Guo, Parimala Vedula, Ryder Li, Michael Potanin, Nidhi Soley, April Yujie Yan, Ishan Vatsaraj, Carl Harris and 4 more

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 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.

Trinity ChengJohns Hopkins University, Department of Biomedical Engineering, Baltimore, 21218, USA.
Shaili TripathiJohns Hopkins University, Department of Biomedical Engineering, Baltimore, 21218, USA.
Yike GuoJohns Hopkins University, Department of Biomedical Engineering, Baltimore, 21218, USA.
Parimala VedulaJohns Hopkins University, Department of Biomedical Engineering, Baltimore, 21218, USA.
Ryder LiJohns Hopkins University, Department of Biomedical Engineering, Baltimore, 21218, USA.
Michael PotaninJohns Hopkins University, Department of Biomedical Engineering, Baltimore, 21218, USA.
Nidhi SoleyJohns Hopkins University, Department of Biomedical Engineering, Baltimore, 21218, USA.
April Yujie YanJohns Hopkins University, Department of Biomedical Engineering, Baltimore, 21218, USA.
Ishan VatsarajJohns Hopkins University, Department of Biomedical Engineering, Baltimore, 21218, USA.
Carl HarrisJohns Hopkins University, Department of Biomedical Engineering, Baltimore, 21218, USA.
Joseph L GreensteinJohns Hopkins University, Department of Biomedical Engineering, Baltimore, 21218, USA.ORCID 0000-0002-6193-7134
Casey Overby TaylorJohns Hopkins University, Department of Biomedical Engineering, Baltimore, 21218, USA.ORCID 0000-0001-9302-5968
Alyssa N CoyneBrain Science Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Jeffrey D RothsteinBrain Science Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.ORCID 0000-0003-2001-8470

Funding

Nuclear and Glial Dysfunction in NeurodegenerationR35NS132179 · NINDS · JOHNS HOPKINS UNIVERSITY · PI Jeffrey D Rothstein · 2023 to 2026
$4.9M
Nuclear pore complex quality control in ALS/FTDR01NS122236 · NINDS · JOHNS HOPKINS UNIVERSITY · PI LUSK, CHARLES PATRICK, ROTHSTEIN, JEFFREY D · 2021 to 2025
$4.0M
NINDS NIH HHS R01 NS122236NINDS NIH HHS R35 NS132179
6 · The paper itself

Abstract

Background: Amyotrophic lateral sclerosis (ALS) is a uniformly fatal neurodegenerative disease characterized by progressive cortical and spinal motor neuron loss, with most patients surviving only 2-5 years post-diagnosis. While approximately 10% of cases are familial (fALS), the remaining 90% are sporadic (sALS) with unknown genetic drivers. Importantly, clinical presentations are heterogeneous in both sporadic and familial ALS, underscoring the complexity of the disease. A pathological hallmark of ALS is the mislocalization of RNA-binding protein TDP-43 from the nucleus to the cytoplasm. This mislocalization produces both loss of function consequences, such as widespread RNA processing and splicing defects, as well as potential toxic gain of function effects associated with cytoplasmic aggregation. Results: In this study, we used RT-PCR data from induced pluripotent stem cell-derived motor neurons derived from 180 sALS and C9orf72 fALS patients from the Answer ALS collection to identify biological subgroups based on TDP-43 loss-of-function signatures. Spectral embedding revealed four distinct molecular clusters, including one subgroup genetically similar to controls and another with the most dysregulated mRNA expression, suggesting differing disease severity. Linear mixed models were then used to assess the longitudinal trajectory of over 90 clinical measures, and the between-cluster interaction effects were evaluated. Conclusions: 36 clinical outcomes showed significant differences across clusters, supporting the presence of biologically and clinically distinct ALS subtypes based on the TDP-43 associated pathogenic cascade. These findings demonstrate a critical role of RNA profiling in uncovering biologically meaningful subtypes of ALS, potentially allowing for more precise prognostic tools and the development of future personalized therapeutic approaches.

Identifiers

PMID41542616
PMCPMC12803177

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