<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><submitter>Lie IA</submitter><funding>Neuro-SysMed at Haukeland University Hospital</funding><funding>Pronova Biocare</funding><funding>Amersham Health</funding><funding>University of Bergen</funding><funding>Dutch MS Research Foundation</funding><funding>Merck Serono, Norway</funding><funding>Helse Vest</funding><funding>Research Council of Norway</funding><funding>National Institute for Health Research (NIHR) biomedical research centre at University College London Hospitals NHS Foundation Trust</funding><funding>Norwegian Multiple Sclerosis Society</funding><funding>Novartis</funding><pubmed_abstract>&lt;h4>Background&lt;/h4>The predictive value of serum neurofilament light chain (sNfL) on long-term prognosis in multiple sclerosis (MS) is still unclear.&lt;h4>Objective&lt;/h4>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.&lt;h4>Methods&lt;/h4>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.&lt;h4>Results&lt;/h4>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.&lt;h4>Conclusion&lt;/h4>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.</pubmed_abstract><journal>Journal of neurology, neurosurgery, and psychiatry</journal><pagination>jnnp-2021-328568</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9304101</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Serum neurofilament as a predictor of 10-year grey matter atrophy and clinical disability in multiple sclerosis: a longitudinal study.</pubmed_title><pmcid>PMC9304101</pmcid><funding_grant_id>MS 18-358f</funding_grant_id><funding_grant_id>912020</funding_grant_id><funding_grant_id>288164</funding_grant_id><pubmed_authors>Holmoy T</pubmed_authors><pubmed_authors>Myhr KM</pubmed_authors><pubmed_authors>Bo L</pubmed_authors><pubmed_authors>Midgard R</pubmed_authors><pubmed_authors>Harbo HF</pubmed_authors><pubmed_authors>Kacar S</pubmed_authors><pubmed_authors>Barkhof F</pubmed_authors><pubmed_authors>Gosal S</pubmed_authors><pubmed_authors>Kvistad SS</pubmed_authors><pubmed_authors>Wergeland S</pubmed_authors><pubmed_authors>Vedeler CA</pubmed_authors><pubmed_authors>Bru A</pubmed_authors><pubmed_authors>Wesnes K</pubmed_authors><pubmed_authors>Kleveland G</pubmed_authors><pubmed_authors>Lie IA</pubmed_authors><pubmed_authors>Brouwer I</pubmed_authors><pubmed_authors>Vrenken H</pubmed_authors><pubmed_authors>Oksendal N</pubmed_authors><pubmed_authors>Torkildsen O</pubmed_authors><pubmed_authors>Edland A</pubmed_authors><pubmed_authors>Sorenes YS</pubmed_authors><pubmed_authors>Eikeland R</pubmed_authors><pubmed_authors>Teunissen CE</pubmed_authors><pubmed_authors>Varhaug KN</pubmed_authors></additional><is_claimable>false</is_claimable><name>Serum neurofilament as a predictor of 10-year grey matter atrophy and clinical disability in multiple sclerosis: a longitudinal study.</name><description>&lt;h4>Background&lt;/h4>The predictive value of serum neurofilament light chain (sNfL) on long-term prognosis in multiple sclerosis (MS) is still unclear.&lt;h4>Objective&lt;/h4>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.&lt;h4>Methods&lt;/h4>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.&lt;h4>Results&lt;/h4>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.&lt;h4>Conclusion&lt;/h4>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.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jun</publication><modification>2026-06-21T03:19:37.899Z</modification><creation>2026-06-21T03:12:35.323Z</creation></dates><accession>S-EPMC9304101</accession><cross_references><pubmed>35649699</pubmed><doi>10.1136/jnnp-2021-328568</doi></cross_references></HashMap>