Abstract

Serum neurofilament light chain (NfL) has been shown to correlate with neuroaxonal damage in multiple sclerosis (MS) and various other neurological diseases. While serum NfL is now regularly reported in clinical approval studies, there is a lack of longitudinal data from patients treated with established basic immunotherapies outside of study conditions. In total, 34 patients with early relapsing-remitting MS (RRMS) were included. The follow-up period was 24 months with regular follow-up visits after 3, 6, 9, 12 and 18 months. Therapy with glatiramer acetate was initiated in 20 patients and with interferon-beta in 12 patients. The disease course was monitored by the events of relapses, Expanded Disability Status Scale (EDSS) score and MRI parameters. Overall, serum NfL levels were higher at time points with a current relapse event than at time points without relapse (12.8 pg/mL vs. 9.7 pg/mL, p = 0.011). At follow-up, relapse-free patients showed significantly reduced serum NfL levels starting from 9 months compared to baseline (p < 0.05) and reduced levels after 12 months compared to baseline (p = 0.013) in patients without EDSS progression for 12 months. In this explorative observational study, our data suggest that the longitudinal measurement of serum NfL may be useful in addition to MRI to monitor disease activity and therapy response.

Highlights

  • Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS)characterized by demyelination and axonal loss [1]

  • The current concept of MS pathology is based on infiltrating immune B- and T-cells via the blood–brain barrier, local antibody production and activation of glial cells [2,3]

  • These processes are thought to lead to primary demyelination followed by neurodegeneration [2]

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Summary

Introduction

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS)characterized by demyelination and axonal loss [1]. The current concept of MS pathology is based on infiltrating immune B- and T-cells via the blood–brain barrier, local antibody production and activation of glial cells [2,3]. These processes are thought to lead to primary demyelination followed by neurodegeneration [2]. Biomedicines 2020, 8, 312 markers for neuroaxonal loss is neurofilament light chain (NfL) [4,5,6]. NfL is one of four neurofilament subunits and the most abundant one, making it a popular target for neurological diseases [7]. NfL showed superior sensitivity for MS than the phosphorylated subunit of neurofilament [8]

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