Evidence map›Paper›PMID 41610159›Full record

ArticlePloS one2026

Retrospective analysis of neurofilament-light chain in patients with inflammatory bowel disease - A pilot study.

Andreas Wolff, Emily Feneberg, Julius Shakhtour, Katja Steiger, Roland M Schmid, Bernhard Haller, Nya Reinhardt, Moritz Middelhoff, David Schult-Hannemann, Paul Lingor

Abstract read
In one paragraph

Article in PloS one, 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

10 authors.

Andreas WolffClinical Department of Neurology, School of Medicine and Health, Technical University of Munich, Munich, Germany.ORCID https://orcid.org/0000-0003-3261-179X
Emily FenebergClinical Department of Neurology, School of Medicine and Health, Technical University of Munich, Munich, Germany.
Julius ShakhtourDepartment of Preclinical Medicine, Institute of Pathology, School of Medicine and Health, School of Medicine and Health, Technical University of Munich, Munich, Germany.
Katja SteigerDepartment of Preclinical Medicine, Institute of Pathology, School of Medicine and Health, School of Medicine and Health, Technical University of Munich, Munich, Germany.ORCID https://orcid.org/0000-0002-7269-5433
Roland M SchmidDepartment of Internal Medicine II, School of Medicine and Health, Technical University of Munich, Munich, Germany.
Bernhard HallerInstitute for AI and Informatics in Medicine, School of Medicine and Health, Technical University of Munich, Munich, Germany.
Nya ReinhardtClinical Department of Neurology, School of Medicine and Health, Technical University of Munich, Munich, Germany.
Moritz MiddelhoffDepartment of Internal Medicine II, School of Medicine and Health, Technical University of Munich, Munich, Germany.
David Schult-HannemannDepartment of Internal Medicine II, School of Medicine and Health, Technical University of Munich, Munich, Germany.
Paul LingorClinical Department of Neurology, School of Medicine and Health, Technical University of Munich, Munich, Germany.ORCID https://orcid.org/0000-0001-9362-7096

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic inflammatory bowel diseases, encompassing Crohn's disease and ulcerative colitis, are characterized by persistent inflammation of the gastrointestinal tract. While traditionally regarded as confined to the gut, the systemic nature of inflammatory bowel disease has been increasingly recognized. The nervous system has garnered particular attention due to molecular and clinical evidence suggesting a potential interplay between inflammatory bowel disease and neurodegenerative diseases. Inflammatory bowel disease patients have a higher risk of developing neurological disorders such as Parkinson's disease, all-cause dementia, and multiple sclerosis. Still, causative molecular mechanisms are poorly understood. Neurofilament light chain (NfL) has been established as a disease-independent biomarker of axonal damage reflecting neurodegeneration.

methodsIn this pilot study, we assessed molecular evidence of neurodegeneration by measuring serum NfL in a single-molecule array using the HD-X SIMOA platform (Quanterix, MA, USA) and employing correlation with clinical data in forty-nine patients with histopathologically confirmed inflammatory bowel disease. In total, 24 Crohn's disease patients, 25 ulcerative colitis patients, and 23 controls, aged 18-79 years, were included.

resultsWe found an age-dependency of serological NfL levels, however, no apparent differences between disease groups and controls. Crohn's disease patients showed a slower age-dependent incline in serological NfL compared to control subjects (p = 0.03). No correlation of NfL with disease duration, disease severity, or inflammatory bowel disease treatment was found.

conclusionsA slower age-dependent increase in serological NfL levels was found in Crohn's disease patients compared to control subjects. Larger studies assessing additional markers of neurodegeneration may be instrumental in addressing this question in the future.

Indexed as

Colitis, UlcerativeCrohn DiseaseInflammatory Bowel DiseasesNeurofilament ProteinsAdolescentAdultAgedBiomarkersCase-Control StudiesFemaleHumansMaleMiddle AgedPilot ProjectsRetrospective StudiesYoung AdultBiomarkersneurofilament protein LNeurofilament Proteins

Identifiers

PMID41610159
PMCPMC12854413

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.