Exploring CSF neurofilament light as a biomarker for MS in clinical practice; a retrospective registry-based study.


Journal

Multiple sclerosis (Houndmills, Basingstoke, England)
ISSN: 1477-0970
Titre abrégé: Mult Scler
Pays: England
ID NLM: 9509185

Informations de publication

Date de publication:
05 2022
Historique:
pubmed: 17 8 2021
medline: 22 4 2022
entrez: 16 8 2021
Statut: ppublish

Résumé

Neurofilament light (NFL) has been increasingly recognized for prognostic and therapeutic decisions. To validate the utility of cerebrospinal fluid NFL (cNFL) as a biomarker in clinical practice of relapsing-remitting multiple sclerosis (RRMS). RRMS patients ( RRMS with relapse had 4.4 times higher median cNFL concentration (1134 [interquartile range (IQR) 499-2744] ng/L) than those without relapse (264 [125-537] ng/L, cNFL is a robust and reliable biomarker of disease activity, treatment response, and prediction of disability and conversion from RRMS to SPMS. Our data suggest that cNFL should be included in the assessment of patients at MS-onset.

Sections du résumé

BACKGROUND
Neurofilament light (NFL) has been increasingly recognized for prognostic and therapeutic decisions.
OBJECTIVE
To validate the utility of cerebrospinal fluid NFL (cNFL) as a biomarker in clinical practice of relapsing-remitting multiple sclerosis (RRMS).
METHODS
RRMS patients (
RESULTS
RRMS with relapse had 4.4 times higher median cNFL concentration (1134 [interquartile range (IQR) 499-2744] ng/L) than those without relapse (264 [125-537] ng/L,
CONCLUSIONS
cNFL is a robust and reliable biomarker of disease activity, treatment response, and prediction of disability and conversion from RRMS to SPMS. Our data suggest that cNFL should be included in the assessment of patients at MS-onset.

Identifiants

pubmed: 34392718
doi: 10.1177/13524585211039104
pmc: PMC9024026
doi:

Substances chimiques

Biomarkers 0
Neurofilament Proteins 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

872-884

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Auteurs

Igal Rosenstein (I)

Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska University Hospital, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Markus Axelsson (M)

Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska University Hospital, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Lenka Novakova (L)

Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska University Hospital, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Kaj Blennow (K)

Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden/Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.

Henrik Zetterberg (H)

Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden/Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden/Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, UK/UK Dementia Research Institute, University College London (UCL), London, UK.

Jan Lycke (J)

Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska University Hospital, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

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