Abstract
Original language | English |
---|---|
Article number | heartjnl-2022-328568 |
Pages (from-to) | 849-857 |
Number of pages | 9 |
Journal | Journal of Neurology, Neurosurgery and Psychiatry |
Volume | 93 |
Issue number | 8 |
Early online date | 2022 |
DOIs | |
Publication status | Published - 1 Aug 2022 |
Keywords
- BIOCHEMISTRY
- CLINICAL NEUROLOGY
- MRI
- MULTIPLE SCLEROSIS
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In: Journal of Neurology, Neurosurgery and Psychiatry, Vol. 93, No. 8, heartjnl-2022-328568, 01.08.2022, p. 849-857.
Research output: Contribution to journal › Article › Academic › peer-review
TY - JOUR
T1 - Serum neurofilament as a predictor of 10-year grey matter atrophy and clinical disability in multiple sclerosis
T2 - a longitudinal study
AU - Lie, Ingrid Anne
AU - Kaçar, Sezgi
AU - Wesnes, Kristin
AU - Brouwer, Iman
AU - Kvistad, Silje S.
AU - Wergeland, Stig
AU - Holmøy, Trygve
AU - Midgard, Rune
AU - Bru, Alla
AU - Edland, Astrid
AU - Eikeland, Randi
AU - Gosal, Sonia
AU - Harbo, Hanne F.
AU - Kleveland, Grethe
AU - Sørenes, Yvonne S.
AU - Øksendal, Nina
AU - Varhaug, Kristin N.
AU - Vedeler, Christian A.
AU - Barkhof, Frederik
AU - Teunissen, Charlotte E.
AU - Bø, Lars
AU - Torkildsen, Øivind
AU - Myhr, Kjell-Morten
AU - Vrenken, Hugo
N1 - Funding Information: Competing interests The authors of this manuscript declare no relationships with any companies, whose products or services may be related to the subject matter of the article. AB, SG, GK, YSS, KNV and CAV declares no disclosures relevant to the manuscript. IAL has received research grants from the Meltzer Research Fund, Gerda Meyer Nyquist Guldbrandson & Gert Meyer Nyquists Legat and the Independent Order of Odd Fellows. KW has received unrestricted research grants from Novartis and Biogen, research grant from the Independent Order of Odd Fellows and speaker honoraria from Biogen. IB has received research support from Merck KGaA, Novartis, and Teva. SW has received speaker honoraria from and served on scientific advisory boards for Biogen, Janssen-Cilag, Sanofi and Novartis. SSK received unrestricted research grants from Novartis, Biogen. TH has received speaker honoraria, research support/grants and participated in clinical trials for Biogen, Merck, Sanofi, Bristol Myers Squibb, Roche and Novartis, is member of the scientific board of the Norwegian MS society, and has received financial support from the Research Council of Norway (grant #250864). RM has served on scientific advisory boards for Novartis Norway and Merck and received travel funding and/or speaker honoraria from Biogen, Novartis and Sanofi Genzyme. AE has received speaker honoraria from Biogen, Merck, Sanofi and Novartis. RE has received speaker honoraria from Novartis. HFH has received speaker honoraria from Biogen, Sanofi-Aventis, Merck, Novartis, and Roche. NØ has received speaker honoraria from Biogen, participated in clinical trials for Biogen and Sanofi-Aventis, and has served on a scientific advisory board for Novartis. FB has received compensation for steering/safety committee, activities and consulting services from Roche, Biogen, Merck, Combinostics, Janssen and IXICO. He is co-founder and shareholder of Queen Square Analytics. CET has a collaboration contract with ADx Neurosciences, Quanterix and Eli Lilly, performed contract research or received grants from AC-Immune, Axon Neurosciences, Biogen, Brainstorm Therapeutics, Celgene, EIP Pharma, Eisai, PeopleBio, Roche, Toyama, Vivoryon. She serves on editorial boards of Medidact Neurologie/Springer, Alzheimer Research and Therapy, Neurology: Neuroimmunology & Neuroinflammation, and is editor of a Neuromethods book Springer. LB has received unrestricted research grants to his institution and/or scientific advisory board or speaker honoraria from Almirall, Biogen, Genzyme, Merck, Novartis, Roche and Teva; and has participated in clinical trials organized by Biogen, Merck, Novartis, Roche, and Genzyme. ØT has received research grants and speaker honoraria from Biogen, Roche, Novartis, Merck and Sanofi. KMM has received unrestricted research grants to his institution; scientific advisory board, or speaker honoraria from Almirall, Biogen, Genzyme, Merck, Novartis, Roche, and Teva; and has participated in clinical trials organized by Biogen, Merck, Novartis, and Roche. HV has received research grants from Pfizer, Merck Serono, Novartis and Teva; speaker honoraria from Novartis; and consulting fees from Merck Serono; all funds were paid directly to his institution. Funding Information: Funding This study received no specific funding. The OFAMS baseline study has been funded by Pronova Biocare; Amersham Health, Norway; Merck Serono, Norway; the Western Norway Regional Health Authority; and Norwegian Multiple Sclerosis Society (no award/grant number). The OFAMS follow-up study has received unrestricted research grants from Novartis and The Independent order of Odd Fellows; has been funded by the Western Norway Regional Health Authority (grant number 912020); and has been financial supported by Neuro-SysMed (Center of excellence for clinical treatment research) hosted by Haukeland University Hospital and funded by grants from the Research Council of Norway (grant number 288164). The MS Center Amsterdam is funded through a program grant of the Dutch MS Research Foundation (grant no. MS 18-358f). IB has been supported by the Dutch MS Research Foundation (no award/grant number). FB is supported by the National Institute for Health Research (NIHR) biomedical research centre at University College London Hospitals NHS Foundation Trust (UCLH) (no award/grant number). ØT and K-MM are funded by Neuro-SysMed at Haukeland University Hospital and University of Bergen by grant from the Research Council of Norway (grant number 288164). Publisher Copyright: ©
PY - 2022/8/1
Y1 - 2022/8/1
N2 - Background: The predictive value of serum neurofilament light chain (sNfL) on long-term prognosis in multiple sclerosis (MS) is still unclear. Objective: Investigate the relation between sNfL levels over a 2-year period in patients with relapsing-remitting MS, and clinical disability and grey matter (GM) atrophy after 10 years. Methods: 85 patients, originally enrolled in a multicentre, randomised trial of ω-3 fatty acids, participated in a 10-year follow-up visit. sNfL levels were measured by Simoa quarterly until month 12, and then at month 24. The appearance of new gadolinium-enhancing (Gd+) lesions was assessed monthly between baseline and month 9, and then at months 12 and 24. At the 10-year follow-up visit, brain atrophy measures were obtained using FreeSurfer. Results: Higher mean sNfL levels during early periods of active inflammation (Gd+ lesions present or recently present) predicted lower total (β=-0.399, p=0.040) and deep (β=-0.556, p=0.010) GM volume, lower mean cortical thickness (β=-0.581, p=0.010) and higher T2 lesion count (β=0.498, p=0.018). Of the clinical outcomes, higher inflammatory sNfL levels were associated with higher disability measured by the dominant hand Nine-Hole Peg Test (β=0.593, p=0.004). Mean sNfL levels during periods of remission (no Gd+ lesions present or recently present) did not predict GM atrophy or disability progression. Conclusion: Higher sNfL levels during periods of active inflammation predicted more GM atrophy and specific aspects of clinical disability 10 years later. The findings suggest that subsequent long-term GM atrophy is mainly due to neuroaxonal degradation within new lesions.
AB - Background: The predictive value of serum neurofilament light chain (sNfL) on long-term prognosis in multiple sclerosis (MS) is still unclear. Objective: Investigate the relation between sNfL levels over a 2-year period in patients with relapsing-remitting MS, and clinical disability and grey matter (GM) atrophy after 10 years. Methods: 85 patients, originally enrolled in a multicentre, randomised trial of ω-3 fatty acids, participated in a 10-year follow-up visit. sNfL levels were measured by Simoa quarterly until month 12, and then at month 24. The appearance of new gadolinium-enhancing (Gd+) lesions was assessed monthly between baseline and month 9, and then at months 12 and 24. At the 10-year follow-up visit, brain atrophy measures were obtained using FreeSurfer. Results: Higher mean sNfL levels during early periods of active inflammation (Gd+ lesions present or recently present) predicted lower total (β=-0.399, p=0.040) and deep (β=-0.556, p=0.010) GM volume, lower mean cortical thickness (β=-0.581, p=0.010) and higher T2 lesion count (β=0.498, p=0.018). Of the clinical outcomes, higher inflammatory sNfL levels were associated with higher disability measured by the dominant hand Nine-Hole Peg Test (β=0.593, p=0.004). Mean sNfL levels during periods of remission (no Gd+ lesions present or recently present) did not predict GM atrophy or disability progression. Conclusion: Higher sNfL levels during periods of active inflammation predicted more GM atrophy and specific aspects of clinical disability 10 years later. The findings suggest that subsequent long-term GM atrophy is mainly due to neuroaxonal degradation within new lesions.
KW - BIOCHEMISTRY
KW - CLINICAL NEUROLOGY
KW - MRI
KW - MULTIPLE SCLEROSIS
UR - http://www.scopus.com/inward/record.url?scp=85132388866&partnerID=8YFLogxK
U2 - https://doi.org/10.1136/jnnp-2021-328568
DO - https://doi.org/10.1136/jnnp-2021-328568
M3 - Article
C2 - 35649699
SN - 0022-3050
VL - 93
SP - 849
EP - 857
JO - Journal of Neurology, Neurosurgery and Psychiatry
JF - Journal of Neurology, Neurosurgery and Psychiatry
IS - 8
M1 - heartjnl-2022-328568
ER -