Evidence map›Paper›PMID 42509459›Full record

ArticleJournal of neurology2026

Plasma cardiac troponin T complements neurofilament light chain by reflecting disease phase and phenotypic variation in amyotrophic lateral sclerosis.

Julia Sellin, Linn Öijerstedt, Janina von der Gablentz, Sanharib Chamoun, Ulf Kläppe, Rayomand Press, Kristin Samuelsson, Julian Grosskreutz, Caroline Ingre

Abstract read
In one paragraph

Article in Journal of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

9 authors.

Julia Sellin *Precision Neurology of Neuromuscular and Motor Neuron Diseases, University of Lübeck, Lübeck, Germany.
Linn Öijerstedt *Department of Clinical Neuroscience, Karolinska Institute, K8 Neuro Ingre, 171 77, Stockholm, Sweden. linn.oijerstedt@ki.se.ORCID http://orcid.org/0000-0003-0635-6377
Janina von der GablentzPrecision Neurology of Neuromuscular and Motor Neuron Diseases, University of Lübeck, Lübeck, Germany.
Sanharib ChamounDepartment of Clinical Neuroscience, Karolinska Institute, K8 Neuro Ingre, 171 77, Stockholm, Sweden.
Ulf KläppeDepartment of Clinical Neuroscience, Karolinska Institute, K8 Neuro Ingre, 171 77, Stockholm, Sweden.
Rayomand PressDepartment of Clinical Neuroscience, Karolinska Institute, K8 Neuro Ingre, 171 77, Stockholm, Sweden.
Kristin SamuelssonDepartment of Clinical Neuroscience, Karolinska Institute, K8 Neuro Ingre, 171 77, Stockholm, Sweden.
Julian Grosskreutz *Precision Neurology of Neuromuscular and Motor Neuron Diseases, University of Lübeck, Lübeck, Germany.
Caroline Ingre *Department of Clinical Neuroscience, Karolinska Institute, K8 Neuro Ingre, 171 77, Stockholm, Sweden.

Funding

Deutsche Forschungsgemeinschaft GR 1578/6-1Deutsche Forschungsgemeinschaft GR 1578/9-1Germany`s Excellence Strategy EXC 2167/2 - 390884018
6 · The paper itself

Abstract

backgroundNeurofilament light chain (NfL) is an established marker of neuronal injury and disease aggressiveness in amyotrophic lateral sclerosis (ALS). In contrast, the clinical and biological significance of cardiac troponin T (cTnT) in ALS is not fully understood. We aimed to evaluate the relationship between plasma cTnT and disease aggressiveness, progression stage, and clinical phenotype in comparison with NfL.

methodsPlasma cTnT and cerebrospinal fluid (CSF) NfL were analysed at diagnosis in a population-based cohort of 526 patients with ALS. Disease aggressiveness was modelled using the D50 framework, which quantifies the time taken to lose 50% of functional capacity (ALSFRS-R) and normalises individual disease trajectories. Biomarker associations with disease aggressiveness, phase, and clinical variables were assessed through group comparisons, logistic and linear regression, and receiver operating characteristic analyses.

resultsNeurofilament light chain in CSF was strongly associated with disease aggressiveness, with higher levels in patients with more aggressive disease. In contrast, plasma hs-cTnT did not correlate with D50. Across disease phases, CSF NfL remained relatively stable, whereas plasma hs-cTnT increased with advancing rD50, suggesting accumulation with disease progression. Plasma hs-cTnT levels were higher in patients with spinal compared to bulbar onset. Combined biomarker models improved sensitivity and negative predictive value for identifying less aggressive disease.

conclusionPlasma hs-cTnT and CSF NfL capture distinct but complementary dimensions of ALS pathology. While NfL reflects disease aggressiveness, hs-cTnT aligns with disease phase and clinical phenotype, supporting its use as a complementary biomarker for ALS characterisation and monitoring.

Indexed as

Amyotrophic Lateral SclerosisNeurofilament ProteinsTroponin TAdultAgedBiomarkersCohort StudiesDisease ProgressionFemaleHumansMaleMiddle AgedPhenotypeBiomarkersneurofilament protein LNeurofilament ProteinsTroponin TAmyotrophic lateral sclerosisD50-ModelDisease aggressivenessNeurofilamentProgressionTroponin-T

Identifiers

PMID42509459
PMCPMC13407708

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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.