Serum neurofilament light for detecting disease activity in individual patients in multiple sclerosis: A 48-week prospective single-center study

Author:

Johnsson M123ORCID,Stenberg YT4,Farman HH5,Blennow K56,Zetterberg H56789,Malmeström C12310,Sandgren S123ORCID,Rosenstein I123ORCID,Lycke J123ORCID,Axelsson M123,Novakova L123ORCID

Affiliation:

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

2. Sahlgrenska University Hospital, Gothenburg, Sweden

3. Department of Neurology, Sahlgrenska University Hospital and Region Västra Götaland, Gothenburg, Sweden

4. Institute of Medicine, University of Gothenburg, Gothenburg, Sweden

5. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden

6. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden

7. UK Dementia Research Institute, University College London, London, UK

8. Hong Kong Center for Neurodegenerative Diseases, Hong Kong, China

9. Wisconsin Alzheimer’s Disease Research Center, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA

10. Laboratory for Clinical Immunology, Department of Neurology, Sahlgrenska University Hospital, Gothenburg, Sweden

Abstract

Background: Serum neurofilament light (sNfL) reflects neuroaxonal damage and is now used as an outcome in treatment trials of relapsing-remitting multiple sclerosis (RRMS). However, the diagnostic properties of sNfL for monitoring disease activity in individual patients warrant further investigations. Method: Patients with suspected relapse and/or contrast-enhancing lesions (CELs) were consecutively included and performed magnetic resonance imaging (MRI) of the brain at baseline and weeks 28 and 48. Serum was obtained at baseline and 2, 4, 8, 16, 24, and 48 weeks. Neurofilament light concentration was measured using Single molecule array technology. Results: We included 44 patients, 40 with RRMS and 4 with clinically isolated syndrome. The median sNfL level peaked at 2 weeks post-baseline (14.6 ng/L, interquartile range (IQR); 9.3–31.6) and reached nadir at 48 weeks (9.1 ng/L, IQR; 5.5–15.0), equivalent to the median sNfL of controls (9.1 ng/L, IQR; 7.4–12). A baseline Z-score of more than 1.1 (area under the curve; 0.78, p < 0.0001) had a sensitivity of 81% and specificity of 70% to detect disease activity. Conclusion: One out of five patients with relapse and/or CELs did not change significantly in post-baseline sNfL levels. The utility of repeated sNfL measurements to monitor disease activity is complementary rather than a substitute for clinical and MRI measures.

Funder

NEURO Sweden

Göteborg Foundation for Neurological Research

Edit Jacobson Foundation

Rune and Ulla Amlövs Foundation for Neurological Research

Swedish Federal Government

Research Foundation of the Multiple Sclerosis Society of Gothenburg/NEURO Gothenburg

Publisher

SAGE Publications

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