Glial fibrillary acidic protein and multiple sclerosis progression independent of acute inflammation.


Journal

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

Informations de publication

Date de publication:
08 2023
Historique:
medline: 10 8 2023
pubmed: 15 6 2023
entrez: 15 6 2023
Statut: ppublish

Résumé

The clinical relevance of serum glial fibrillary acidic protein (sGFAP) concentration as a biomarker of MS disability progression independent of acute inflammation has yet to be quantified. To test whether baseline values and longitudinal changes in sGFAP concentration are associated with disability progression without detectable relapse of magnetic resonance imaging (MRI) inflammatory activity in participants with secondary-progressive multiple sclerosis (SPMS). We retrospectively analyzed longitudinal sGFAP concentration and clinical outcome data from the Phase 3 ASCEND trial of participants with SPMS, with no detectable relapse or MRI signs of inflammatory activity at baseline nor during the study ( We found a significant cross-sectional association between baseline sGFAP and sNfL concentrations and T2 lesion volume. No or weak correlations between sGFAP concentration and changes in EDSS, T25FW, and 9HPT, or CDP were observed. Without inflammatory activity, changes in sGFAP concentration in participants with SPMS were neither associated with current nor predictive of future disability progression.

Sections du résumé

BACKGROUND
The clinical relevance of serum glial fibrillary acidic protein (sGFAP) concentration as a biomarker of MS disability progression independent of acute inflammation has yet to be quantified.
OBJECTIVE
To test whether baseline values and longitudinal changes in sGFAP concentration are associated with disability progression without detectable relapse of magnetic resonance imaging (MRI) inflammatory activity in participants with secondary-progressive multiple sclerosis (SPMS).
METHODS
We retrospectively analyzed longitudinal sGFAP concentration and clinical outcome data from the Phase 3 ASCEND trial of participants with SPMS, with no detectable relapse or MRI signs of inflammatory activity at baseline nor during the study (
RESULTS
We found a significant cross-sectional association between baseline sGFAP and sNfL concentrations and T2 lesion volume. No or weak correlations between sGFAP concentration and changes in EDSS, T25FW, and 9HPT, or CDP were observed.
CONCLUSION
Without inflammatory activity, changes in sGFAP concentration in participants with SPMS were neither associated with current nor predictive of future disability progression.

Identifiants

pubmed: 37317870
doi: 10.1177/13524585231176732
pmc: PMC10413790
doi:

Substances chimiques

Glial Fibrillary Acidic Protein 0
Biomarkers 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1070-1079

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Auteurs

Xiaotong Jiang (X)

Biogen, Cambridge, MA, USA.

Changyu Shen (C)

Biogen, Cambridge, MA, USA.

Charlotte E Teunissen (CE)

Neurochemistry Laboratory, Department of Clinical Chemistry, Amsterdam Neuroscience, Program Neuroinflammation, Amsterdam UMC, Vrije Universiteit, Amsterdam, The Netherlands/Department of Neurology, Amsterdam Neuroscience, Program Neuroinflammation, Amsterdam UMC, Vrije Universiteit, Amsterdam, The Netherlands.

Mark Wessels (M)

MS Center Amsterdam, Department of Neurology, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit, Amsterdam, The Netherlands.

Henrik Zetterberg (H)

Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, MöIndal, Sweden/Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, MöIndal, Sweden/Department of Neurodegenerative Disease, UCL Institute of Neurology, London, UK/UK Dementia Research Institute at UCL, London, UK/Hong Kong Center for Neurodegenerative Diseases, Hong Kong, China.

Gavin Giovannoni (G)

Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.

Carol M Singh (CM)

Biogen, Cambridge, MA, USA.

Bastien Caba (B)

Biogen, Cambridge, MA, USA.

Colm Elliott (C)

NeuroRx, Montreal, QC, Canada.

Elizabeth Fisher (E)

Biogen, Cambridge, MA, USA.

Carl de Moor (C)

Biogen, Cambridge, MA, USA.

Shibeshih Belachew (S)

Biogen, Cambridge, MA, USA.

Arie R Gafson (AR)

Biogen, Cambridge, MA, USA.

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Classifications MeSH