Evidence map›Paper›PMID 41450782›Full record

ArticleMolecular neurodegeneration advances2026

Serum metabolomic-lipidomic signatures track long-term neurological performance in multiple sclerosis.

Rose Noroozi, Hui-Hsin Tsai, Ketian Yu, Karunakar Samuel, Kien Trinh, Ellen A Tsai, Farren B S Briggs, Pavan Bhargava, Kathryn C Fitzgerald

Abstract read
In one paragraph

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

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0citing papers in PubMed
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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

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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

9 authors.

Rose NorooziDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD USA.
Hui-Hsin TsaiMS&I and AD Clinical Development, Biogen, Cambridge, MA USA.
Ketian YuBiomarkers and Systems Biology, Biogen, Cambridge, MA USA.
Karunakar SamuelDepartment of Neuroimmunology, School of Medicine and Dentistry, University of Rochester, Rochester, NY USA.
Kien TrinhBiomarkers and Systems Biology, Biogen, Cambridge, MA USA.
Ellen A TsaiBiomarkers and Systems Biology, Biogen, Cambridge, MA USA.
Farren B S BriggsPublic Health Sciences, University of Miami Miller School of Medicine, Miami, FL USA.
Pavan BhargavaDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD USA.
Kathryn C FitzgeraldDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD USA.

Funding

Metabolic predictors of disease outcomes in multiple sclerosisR01NS133005 · NINDS · JOHNS HOPKINS UNIVERSITY · PI Kathryn C. Fitzgerald · 2024 to 2026
$1.9M
NINDS NIH HHS R01 NS133005
6 · The paper itself

Abstract

Metabolomics incorporates information from multiple biological systems and is recognized as an emerging tool for identifying novel multiple sclerosis (MS) biomarkers. While prior studies have linked metabolic alterations to the disease severity in people with MS (pwMS), a longitudinal approach enables a significant advantage in studying this relationship over disease progression. Therefore, this study aims to identify metabolomic signatures associated with longitudinal outcomes in pwMS. We performed a multi-site study, profiling the serum metabolome (Biocrates Inc.) from participants for the MS Partners Advancing Technology and Health Solutions (MS PATHS) network. Outcomes, including 25-foot walking speed, manual dexterity, and processing speed, were quantified using the iPad®-based Multiple Sclerosis Performance Test (MSPT). We applied generalized estimating equation regression models (adjusted for potential confounders) to assess the association of 517 metabolites at baseline with longitudinal assessments of MSPT component tests. We performed network, pathway enrichment, and MetaboIndicator analyses to infer biological insights from our findings. This study included 767 pwMS (mean age 44.9 [SD: 11.4]; 72.1% relapsing-remitting MS; 72.9% female; 11.8% non-white), who had an average of 7.0 (SD = 4.57) MSPT measures per person over an average follow-up period of 3.0 (SD = 1.25) years. Certain metabolites were associated with MSPT outcomes over time. For example, a 1 SD decrease in Phosphatidyl-choline aa C36:6 (PC aa 36:6) level was associated with a 9.3% decline in walking speed performance (95% CI: 6.7-11.9; FDR-adjusted p = 8.9E-09) and a 5.4% reduction in manual dexterity performance (95% CI: 3.3-7.4; FDR-adjusted p = 9.6E-05). Metabolite set enrichment and MetaboIndicator analyses pointed to pathways involved in polyunsaturated fatty acid (PUFA) metabolism and suggested altered enzymatic activities, such as increased phospholipase A2 (PLA2) activity. Leveraging a large longitudinal cohort, our findings suggest a potential role of altered lipid metabolism in the progression of MS. Supplementary Information: The online version contains supplementary material available at 10.1186/s44477-025-00008-7.

Indexed as

Biofluid BiomarkersCognitive testingLipidomicsMetabolomicsMultiple SclerosisNeurological functioning

Identifiers

PMID41450782
PMCPMC12727765

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.