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Serum Neurofilament Light and Glial Fibrillary Acidic Protein Levels Are Not Associated with Wearing-off Symptoms in Natalizumab-treated Multiple Sclerosis Patients

Overview
Journal Mult Scler
Publisher Sage Publications
Specialty Neurology
Date 2024 Nov 4
PMID 39494701
Authors
Alyssa A Toorop
Mark Hj Wessels
Lynn Boonkamp
Liza My Gelissen
E Hoitsma
Esther Mpe Zeinstra
Luuk C van Rooij
Caspar Ep van Munster
Anke Vennegoor
Jop P Mostert
Beatrijs Ha Wokke
Nynke F Kalkers
Erwin Lj Hoogervorst
Jeroen Jj van Eijk
Christiaan M Roosendaal
Jolijn J Kragt
Marijke Eurelings
Jessie van Genugten
Jessica Nielsen
Lgf Sinnige
Mark E Kloosterziel
Edo Pj Arnoldus
Gert W van Dijk
Willem H Bouvy
Eva Mm Strijbis
Bob W van Oosten
Brigit A de Jong
Bernard Mj Uitdehaag
Theo Rispens
Joep Killestein
Zoe LE van Kempen
Charlotte E Teunissen
Affiliations
Soon will be listed here.
Abstract

Background: Biomarkers of neuronal and axonal damage (serum neurofilament light (sNfL) and serum glial fibrillary acidic protein (sGFAP)) may provide insight into the aetiology of natalizumab wearing-off symptoms (WoSs).

Objectives: We investigated the longitudinal association between and predictive value of sNfL and sGFAP and the occurrence of WoS in MS patients treated with natalizumab.

Methods: We performed longitudinal measurements of sNfL and sGFAP in NEXT-MS trial participants who completed a questionnaire about WoS.

Results: A total of 364 participants were included. In total, 55.5% presented with WoS and 44.5% without WoS during natalizumab treatment. Longitudinal analyses showed no association between sNfL and sGFAP levels and WoS at any timepoint. Biomarker levels at baseline did not predict first-time WoS occurrence.

Conclusion: Acute and chronic neuronal and axonal damage are most likely not the underlying cause of WoS.

Citing Articles

Effect of Natalizumab on sNfL and sGFAP Levels in Multiple Sclerosis Patients.

Sainz-Amo R, Rodero-Romero A, Monreal E, Chico-Garcia J, Rodriguez-Jorge F, Fernandez-Velasco J Int J Mol Sci. 2024; 25(23).

PMID: 39684862 PMC: 11642535. DOI: 10.3390/ijms252313153.

References
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