Serum neurofilament light chain levels at attack predict post-attack disability worsening and are mitigated by inebilizumab: analysis of four potential biomarkers in neuromyelitis optica spectrum disorder
ObjectiveTo investigate relationships between serum neurofilament light chain (sNfL), ubiquitin C-terminal hydrolase L1 (sUCHL1), tau (sTau) and glial fibrillary acidic protein (sGFAP) levels and disease activity/disability in neuromyelitis optica spectrum disorder (NMOSD), and the effects of inebil...
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| Veröffentlicht in: | Journal of Neurology, Neurosurgery & Psychiatry Jg. 94; H. 9; S. 757 - 768 |
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| Format: | Journal Article |
| Sprache: | Englisch |
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England
BMJ Publishing Group Ltd
01.09.2023
BMJ BMJ Publishing Group LTD BMJ Publishing Group |
| Schriftenreihe: | Original research |
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| ISSN: | 0022-3050, 1468-330X, 1468-330X |
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| Abstract | ObjectiveTo investigate relationships between serum neurofilament light chain (sNfL), ubiquitin C-terminal hydrolase L1 (sUCHL1), tau (sTau) and glial fibrillary acidic protein (sGFAP) levels and disease activity/disability in neuromyelitis optica spectrum disorder (NMOSD), and the effects of inebilizumab on these biomarkers in N-MOmentum.MethodsN-MOmentum randomised participants to receive inebilizumab or placebo with a randomised controlled period (RCP) of 28 weeks and an open-label follow-up period of ≥2 years. The sNfL, sUCHL1, sTau and sGFAP were measured using single-molecule arrays in 1260 scheduled and attack-related samples from N-MOmentum participants (immunoglobulin G (IgG) autoantibodies to aquaporin-4-positive, myelin oligodendrocyte glycoprotein-IgG-positive or double autoantibody-negative) and two control groups (healthy donors and patients with relapsing–remitting multiple sclerosis).ResultsThe concentration of all four biomarkers increased during NMOSD attacks. At attack, sNfL had the strongest correlation with disability worsening during attacks (Spearman R2=0.40; p=0.01) and prediction of disability worsening after attacks (sNfL cut-off 32 pg/mL; area under the curve 0.71 (95% CI 0.51 to 0.89); p=0.02), but only sGFAP predicted upcoming attacks. At RCP end, fewer inebilizumab-treated than placebo-treated participants had sNfL>16 pg/mL (22% vs 45%; OR 0.36 (95% CI 0.17 to 0.76); p=0.004).ConclusionsCompared with sGFAP, sTau and sUCHL1, sNfL at attack was the strongest predictor of disability worsening at attack and follow-up, suggesting a role for identifying participants with NMOSD at risk of limited post-relapse recovery. Treatment with inebilizumab was associated with lower levels of sGFAP and sNfL than placebo.Trial registration number NCT02200770. |
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| AbstractList | ObjectiveTo investigate relationships between serum neurofilament light chain (sNfL), ubiquitin C-terminal hydrolase L1 (sUCHL1), tau (sTau) and glial fibrillary acidic protein (sGFAP) levels and disease activity/disability in neuromyelitis optica spectrum disorder (NMOSD), and the effects of inebilizumab on these biomarkers in N-MOmentum.MethodsN-MOmentum randomised participants to receive inebilizumab or placebo with a randomised controlled period (RCP) of 28 weeks and an open-label follow-up period of ≥2 years. The sNfL, sUCHL1, sTau and sGFAP were measured using single-molecule arrays in 1260 scheduled and attack-related samples from N-MOmentum participants (immunoglobulin G (IgG) autoantibodies to aquaporin-4-positive, myelin oligodendrocyte glycoprotein-IgG-positive or double autoantibody-negative) and two control groups (healthy donors and patients with relapsing–remitting multiple sclerosis).ResultsThe concentration of all four biomarkers increased during NMOSD attacks. At attack, sNfL had the strongest correlation with disability worsening during attacks (Spearman R2=0.40; p=0.01) and prediction of disability worsening after attacks (sNfL cut-off 32 pg/mL; area under the curve 0.71 (95% CI 0.51 to 0.89); p=0.02), but only sGFAP predicted upcoming attacks. At RCP end, fewer inebilizumab-treated than placebo-treated participants had sNfL>16 pg/mL (22% vs 45%; OR 0.36 (95% CI 0.17 to 0.76); p=0.004).ConclusionsCompared with sGFAP, sTau and sUCHL1, sNfL at attack was the strongest predictor of disability worsening at attack and follow-up, suggesting a role for identifying participants with NMOSD at risk of limited post-relapse recovery. Treatment with inebilizumab was associated with lower levels of sGFAP and sNfL than placebo.Trial registration numberNCT02200770. To investigate relationships between serum neurofilament light chain (sNfL), ubiquitin C-terminal hydrolase L1 (sUCHL1), tau (sTau) and glial fibrillary acidic protein (sGFAP) levels and disease activity/disability in neuromyelitis optica spectrum disorder (NMOSD), and the effects of inebilizumab on these biomarkers in N-MOmentum. N-MOmentum randomised participants to receive inebilizumab or placebo with a randomised controlled period (RCP) of 28 weeks and an open-label follow-up period of ≥2 years. The sNfL, sUCHL1, sTau and sGFAP were measured using single-molecule arrays in 1260 scheduled and attack-related samples from N-MOmentum participants (immunoglobulin G (IgG) autoantibodies to aquaporin-4-positive, myelin oligodendrocyte glycoprotein-IgG-positive or double autoantibody-negative) and two control groups (healthy donors and patients with relapsing-remitting multiple sclerosis). The concentration of all four biomarkers increased during NMOSD attacks. At attack, sNfL had the strongest correlation with disability worsening during attacks (Spearman R =0.40; p=0.01) and prediction of disability worsening after attacks (sNfL cut-off 32 pg/mL; area under the curve 0.71 (95% CI 0.51 to 0.89); p=0.02), but only sGFAP predicted upcoming attacks. At RCP end, fewer inebilizumab-treated than placebo-treated participants had sNfL>16 pg/mL (22% vs 45%; OR 0.36 (95% CI 0.17 to 0.76); p=0.004). Compared with sGFAP, sTau and sUCHL1, sNfL at attack was the strongest predictor of disability worsening at attack and follow-up, suggesting a role for identifying participants with NMOSD at risk of limited post-relapse recovery. Treatment with inebilizumab was associated with lower levels of sGFAP and sNfL than placebo. NCT02200770. To investigate relationships between serum neurofilament light chain (sNfL), ubiquitin C-terminal hydrolase L1 (sUCHL1), tau (sTau) and glial fibrillary acidic protein (sGFAP) levels and disease activity/disability in neuromyelitis optica spectrum disorder (NMOSD), and the effects of inebilizumab on these biomarkers in N-MOmentum.OBJECTIVETo investigate relationships between serum neurofilament light chain (sNfL), ubiquitin C-terminal hydrolase L1 (sUCHL1), tau (sTau) and glial fibrillary acidic protein (sGFAP) levels and disease activity/disability in neuromyelitis optica spectrum disorder (NMOSD), and the effects of inebilizumab on these biomarkers in N-MOmentum.N-MOmentum randomised participants to receive inebilizumab or placebo with a randomised controlled period (RCP) of 28 weeks and an open-label follow-up period of ≥2 years. The sNfL, sUCHL1, sTau and sGFAP were measured using single-molecule arrays in 1260 scheduled and attack-related samples from N-MOmentum participants (immunoglobulin G (IgG) autoantibodies to aquaporin-4-positive, myelin oligodendrocyte glycoprotein-IgG-positive or double autoantibody-negative) and two control groups (healthy donors and patients with relapsing-remitting multiple sclerosis).METHODSN-MOmentum randomised participants to receive inebilizumab or placebo with a randomised controlled period (RCP) of 28 weeks and an open-label follow-up period of ≥2 years. The sNfL, sUCHL1, sTau and sGFAP were measured using single-molecule arrays in 1260 scheduled and attack-related samples from N-MOmentum participants (immunoglobulin G (IgG) autoantibodies to aquaporin-4-positive, myelin oligodendrocyte glycoprotein-IgG-positive or double autoantibody-negative) and two control groups (healthy donors and patients with relapsing-remitting multiple sclerosis).The concentration of all four biomarkers increased during NMOSD attacks. At attack, sNfL had the strongest correlation with disability worsening during attacks (Spearman R2=0.40; p=0.01) and prediction of disability worsening after attacks (sNfL cut-off 32 pg/mL; area under the curve 0.71 (95% CI 0.51 to 0.89); p=0.02), but only sGFAP predicted upcoming attacks. At RCP end, fewer inebilizumab-treated than placebo-treated participants had sNfL>16 pg/mL (22% vs 45%; OR 0.36 (95% CI 0.17 to 0.76); p=0.004).RESULTSThe concentration of all four biomarkers increased during NMOSD attacks. At attack, sNfL had the strongest correlation with disability worsening during attacks (Spearman R2=0.40; p=0.01) and prediction of disability worsening after attacks (sNfL cut-off 32 pg/mL; area under the curve 0.71 (95% CI 0.51 to 0.89); p=0.02), but only sGFAP predicted upcoming attacks. At RCP end, fewer inebilizumab-treated than placebo-treated participants had sNfL>16 pg/mL (22% vs 45%; OR 0.36 (95% CI 0.17 to 0.76); p=0.004).Compared with sGFAP, sTau and sUCHL1, sNfL at attack was the strongest predictor of disability worsening at attack and follow-up, suggesting a role for identifying participants with NMOSD at risk of limited post-relapse recovery. Treatment with inebilizumab was associated with lower levels of sGFAP and sNfL than placebo.CONCLUSIONSCompared with sGFAP, sTau and sUCHL1, sNfL at attack was the strongest predictor of disability worsening at attack and follow-up, suggesting a role for identifying participants with NMOSD at risk of limited post-relapse recovery. Treatment with inebilizumab was associated with lower levels of sGFAP and sNfL than placebo.NCT02200770.TRIAL REGISTRATION NUMBERNCT02200770. ObjectiveTo investigate relationships between serum neurofilament light chain (sNfL), ubiquitin C-terminal hydrolase L1 (sUCHL1), tau (sTau) and glial fibrillary acidic protein (sGFAP) levels and disease activity/disability in neuromyelitis optica spectrum disorder (NMOSD), and the effects of inebilizumab on these biomarkers in N-MOmentum.MethodsN-MOmentum randomised participants to receive inebilizumab or placebo with a randomised controlled period (RCP) of 28 weeks and an open-label follow-up period of ≥2 years. The sNfL, sUCHL1, sTau and sGFAP were measured using single-molecule arrays in 1260 scheduled and attack-related samples from N-MOmentum participants (immunoglobulin G (IgG) autoantibodies to aquaporin-4-positive, myelin oligodendrocyte glycoprotein-IgG-positive or double autoantibody-negative) and two control groups (healthy donors and patients with relapsing–remitting multiple sclerosis).ResultsThe concentration of all four biomarkers increased during NMOSD attacks. At attack, sNfL had the strongest correlation with disability worsening during attacks (Spearman R2=0.40; p=0.01) and prediction of disability worsening after attacks (sNfL cut-off 32 pg/mL; area under the curve 0.71 (95% CI 0.51 to 0.89); p=0.02), but only sGFAP predicted upcoming attacks. At RCP end, fewer inebilizumab-treated than placebo-treated participants had sNfL>16 pg/mL (22% vs 45%; OR 0.36 (95% CI 0.17 to 0.76); p=0.004).ConclusionsCompared with sGFAP, sTau and sUCHL1, sNfL at attack was the strongest predictor of disability worsening at attack and follow-up, suggesting a role for identifying participants with NMOSD at risk of limited post-relapse recovery. Treatment with inebilizumab was associated with lower levels of sGFAP and sNfL than placebo.Trial registration number NCT02200770. |
| Author | Marignier, Romain Weinshenker, Brian G Cree, Bruce A Aktas, Orhan Gunsior, Michele Fujihara, Kazuo Rees, William A Pittock, Sean J Cutter, Gary Bennett, Jeffrey L Wingerchuk, Dean M Paul, Friedemann She, Dewei Katz, Eliezer Hartung, Hans-Peter Smith, Michael A Cimbora, Daniel Kim, Ho Jin |
| AuthorAffiliation | 5 Horizon Therapeutics plc , Gaithersburg , Maryland , USA 10 Departments of Neurology and Ophthalmology, Programs in Neuroscience and Immunology , University of Colorado - Anschutz Medical Campus , Aurora , Colorado , USA 9 Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation , Hopital Neurologique et Neurochirurgical Pierre Wertheimer Centre de reference des syndromes neurologiques paraneoplasiques et encephalites auto-immun , Lyon , Auvergne-Rhône-Alpes , France 16 Department of Neurology , UCSF, Weill Institute for Neurosciences, University California of San Francisco , San Francisco , California , USA 7 Multiple Sclerosis and Neuromyelitis Optica Center , Southern Tohoku Research Institute for Neuroscience , Koriyama , Japan 1 Department of Neurology, Medical Faculty , Heinrich Heine University Düsseldorf , Düsseldorf , Germany 11 Department of Neurology , Re |
| AuthorAffiliation_xml | – name: 14 Department of Neurology , Mayo Clinic , Scottsdale , Arizona , USA – name: 2 Brain and Mind Centre , University of Sydney , Sydney , New South Wales , Australia – name: 3 Department of Neurology , Medical University Vienna , Vienna , Austria – name: 10 Departments of Neurology and Ophthalmology, Programs in Neuroscience and Immunology , University of Colorado - Anschutz Medical Campus , Aurora , Colorado , USA – name: 11 Department of Neurology , Research Institute and Hospital of National Cancer Center , Goyang , Republic of Korea – name: 8 Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité , Universitätsmedizin Berlin , Berlin , Germany – name: 9 Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation , Hopital Neurologique et Neurochirurgical Pierre Wertheimer Centre de reference des syndromes neurologiques paraneoplasiques et encephalites auto-immun , Lyon , Auvergne-Rhône-Alpes , France – name: 6 Department of Multiple Sclerosis Therapeutics , Fukushima Medical University , Koriyama , Fukushima , Japan – name: 1 Department of Neurology, Medical Faculty , Heinrich Heine University Düsseldorf , Düsseldorf , Germany – name: 7 Multiple Sclerosis and Neuromyelitis Optica Center , Southern Tohoku Research Institute for Neuroscience , Koriyama , Japan – name: 5 Horizon Therapeutics plc , Gaithersburg , Maryland , USA – name: 13 Department of Neurology and Center for MS and Autoimmune Neurology , Mayo Clinic , Rochester , Minnesota , USA – name: 4 Department of Neurology , Palacky University in Olomouc , Olomouc , Czech Republic – name: 15 Department of Biostatistics , University of Alabama at Birmingham , Birmingham , Alabama , USA – name: 16 Department of Neurology , UCSF, Weill Institute for Neurosciences, University California of San Francisco , San Francisco , California , USA – name: 12 Department of Neurology , University of Virginia , Charlottesville , Virginia , USA |
| Author_xml | – sequence: 1 givenname: Orhan orcidid: 0000-0002-2020-9210 surname: Aktas fullname: Aktas, Orhan email: orhan.aktas@uni organization: Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany – sequence: 2 givenname: Hans-Peter surname: Hartung fullname: Hartung, Hans-Peter organization: Department of Neurology, Palacky University in Olomouc, Olomouc, Czech Republic – sequence: 3 givenname: Michael A surname: Smith fullname: Smith, Michael A organization: Horizon Therapeutics plc, Gaithersburg, Maryland, USA – sequence: 4 givenname: William A surname: Rees fullname: Rees, William A organization: Horizon Therapeutics plc, Gaithersburg, Maryland, USA – sequence: 5 givenname: Kazuo surname: Fujihara fullname: Fujihara, Kazuo organization: Multiple Sclerosis and Neuromyelitis Optica Center, Southern Tohoku Research Institute for Neuroscience, Koriyama, Japan – sequence: 6 givenname: Friedemann surname: Paul fullname: Paul, Friedemann organization: Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité, Universitätsmedizin Berlin, Berlin, Germany – sequence: 7 givenname: Romain surname: Marignier fullname: Marignier, Romain organization: Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Hopital Neurologique et Neurochirurgical Pierre Wertheimer Centre de reference des syndromes neurologiques paraneoplasiques et encephalites auto-immun, Lyon, Auvergne-Rhône-Alpes, France – sequence: 8 givenname: Jeffrey L surname: Bennett fullname: Bennett, Jeffrey L organization: Departments of Neurology and Ophthalmology, Programs in Neuroscience and Immunology, University of Colorado - Anschutz Medical Campus, Aurora, Colorado, USA – sequence: 9 givenname: Ho Jin orcidid: 0000-0002-8672-8419 surname: Kim fullname: Kim, Ho Jin organization: Department of Neurology, Research Institute and Hospital of National Cancer Center, Goyang, Republic of Korea – sequence: 10 givenname: Brian G surname: Weinshenker fullname: Weinshenker, Brian G organization: Department of Neurology, University of Virginia, Charlottesville, Virginia, USA – sequence: 11 givenname: Sean J orcidid: 0000-0002-6140-5584 surname: Pittock fullname: Pittock, Sean J organization: Department of Neurology and Center for MS and Autoimmune Neurology, Mayo Clinic, Rochester, Minnesota, USA – sequence: 12 givenname: Dean M surname: Wingerchuk fullname: Wingerchuk, Dean M organization: Department of Neurology, Mayo Clinic, Scottsdale, Arizona, USA – sequence: 13 givenname: Gary surname: Cutter fullname: Cutter, Gary organization: Department of Biostatistics, University of Alabama at Birmingham, Birmingham, Alabama, USA – sequence: 14 givenname: Dewei surname: She fullname: She, Dewei organization: Horizon Therapeutics plc, Gaithersburg, Maryland, USA – sequence: 15 givenname: Michele surname: Gunsior fullname: Gunsior, Michele organization: Horizon Therapeutics plc, Gaithersburg, Maryland, USA – sequence: 16 givenname: Daniel surname: Cimbora fullname: Cimbora, Daniel organization: Horizon Therapeutics plc, Gaithersburg, Maryland, USA – sequence: 17 givenname: Eliezer surname: Katz fullname: Katz, Eliezer organization: Horizon Therapeutics plc, Gaithersburg, Maryland, USA – sequence: 18 givenname: Bruce A surname: Cree fullname: Cree, Bruce A email: bruce.cree@ucsf.edu organization: Department of Neurology, UCSF, Weill Institute for Neurosciences, University California of San Francisco, San Francisco, California, USA |
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| DOI | 10.1136/jnnp-2022-330412 |
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| Keywords | RANDOMISED TRIALS CLINICAL NEUROLOGY |
| Language | English |
| License | This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/. Author(s) (or their employer(s)) 2023. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. |
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disorder publication-title: Neurol Neuroimmunol Neuroinflamm doi: 10.1212/NXI.0000000000000978 – volume: 18 start-page: 105 year: 2021 ident: 2024102910301110000_94.9.757.39 article-title: Serum GFAP and NFL as disease severity and prognostic biomarkers in patients with aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder publication-title: J Neuroinflammation doi: 10.1186/s12974-021-02138-7 – volume: 78 start-page: 741 year: 2021 ident: 2024102910301110000_94.9.757.25 article-title: Positive predictive value of myelin oligodendrocyte glycoprotein autoantibody testing publication-title: JAMA Neurol doi: 10.1001/jamaneurol.2021.0912 – volume: 3 start-page: 58 year: 2012 ident: 2024102910301110000_94.9.757.2 article-title: Neuromyelitis optica should be classified as an astrocytopathic disease rather than a demyelinating disease publication-title: Clin Exp Neuroimmunol doi: 10.1111/j.1759-1961.2012.00030.x – ident: 2024102910301110000_94.9.757.11 doi: 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10.1016/j.msard.2012.06.002 – volume: 8 year: 2021 ident: 2024102910301110000_94.9.757.19 article-title: Increased serum neurofilament light and thin ganglion cell-inner plexiform layer are additive risk factors for disease activity in early multiple sclerosis publication-title: Neurol Neuroimmunol Neuroinflamm doi: 10.1212/NXI.0000000000001051 – volume: 56 start-page: 102785 year: 2020 ident: 2024102910301110000_94.9.757.30 article-title: Blood biomarkers on admission in acute traumatic brain injury: relations to severity, CT findings and care path in the CENTER-TBI study publication-title: EBioMedicine doi: 10.1016/j.ebiom.2020.102785 – ident: 2024102910301110000_94.9.757.26 doi: 10.1212/WNL.53.5.1107 – volume: 6 start-page: 85 year: 2020 ident: 2024102910301110000_94.9.757.4 article-title: Neuromyelitis optica publication-title: Nat Rev Dis Primers doi: 10.1038/s41572-020-0214-9 – ident: 2024102910301110000_94.9.757.3 doi: 10.1212/01.wnl.0000254502.87233.9a – ident: 2024102910301110000_94.9.757.23 doi: 10.1016/S0140-6736(19)31817-3 – ident: 2024102910301110000_94.9.757.27 doi: 10.1016/S1474-4422(13)70076-0 – ident: 2024102910301110000_94.9.757.36 doi: 10.1136/jnnp-2018-318382 – ident: 2024102910301110000_94.9.757.34 doi: 10.1007/s00415-013-7169-7 – ident: 2024102910301110000_94.9.757.31 – volume: 94 start-page: e407 year: 2020 ident: 2024102910301110000_94.9.757.37 article-title: Longitudinal optic neuritis-unrelated visual evoked potential changes in NMO spectrum disorders publication-title: Neurology doi: 10.1212/WNL.0000000000008684 – ident: 2024102910301110000_94.9.757.18 doi: 10.1136/jnnp-2018-320106 – ident: 2024102910301110000_94.9.757.1 doi: 10.1177/1352458515620934 – volume: 10 year: 2023 ident: 2024102910301110000_94.9.757.40 article-title: Serum GFAP and NFL levels differentiate subsequent progression and disease activity in patients with progressive multiple sclerosis publication-title: Neurol Neuroimmunol Neuroinflamm doi: 10.1212/NXI.0000000000200052 – volume: 145 start-page: 1726 year: 2022 ident: 2024102910301110000_94.9.757.7 article-title: A new form of axonal pathology in a spinal model of neuromyelitis optica publication-title: Brain doi: 10.1093/brain/awac079 – volume: 11 start-page: 730 year: 2019 ident: 2024102910301110000_94.9.757.16 article-title: The diagnostic performance of neurofilament light chain in CSF and blood for alzheimer’s disease, frontotemporal dementia, and amyotrophic lateral sclerosis: a systematic review and meta-analysis publication-title: Alzheimers Dement (Amst) doi: 10.1016/j.dadm.2019.08.009 – ident: 2024102910301110000_94.9.757.33 doi: 10.1002/ana.24554 – volume: 7 year: 2019 ident: 2024102910301110000_94.9.757.6 article-title: Complement-independent bystander injury in AQP4-igG seropositive neuromyelitis optica produced by antibody-dependent cellular cytotoxicity publication-title: Acta Neuropathol Commun doi: 10.1186/s40478-019-0766-7 – volume: 11 year: 2019 ident: 2024102910301110000_94.9.757.21 article-title: Role of tau as a microtubule-associated protein: structural and functional aspects publication-title: Front Aging Neurosci doi: 10.3389/fnagi.2019.00204 – volume: 93 start-page: e1299 year: 2019 ident: 2024102910301110000_94.9.757.13 article-title: Serum GFAP and neurofilament light as biomarkers of disease activity and disability in NMOSD publication-title: Neurology doi: 10.1212/WNL.0000000000008160 – volume: 9 start-page: 1438 year: 2018 ident: 2024102910301110000_94.9.757.8 article-title: Aquaporin-4 autoantibodies from neuromyelitis optica spectrum disorder patients induce complement-independent immunopathologies in mice publication-title: Front Immunol doi: 10.3389/fimmu.2018.01438 |
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| Snippet | ObjectiveTo investigate relationships between serum neurofilament light chain (sNfL), ubiquitin C-terminal hydrolase L1 (sUCHL1), tau (sTau) and glial... To investigate relationships between serum neurofilament light chain (sNfL), ubiquitin C-terminal hydrolase L1 (sUCHL1), tau (sTau) and glial fibrillary acidic... |
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| SubjectTerms | Alzheimer's disease Antibodies, Monoclonal, Humanized - therapeutic use Aquaporin 4 Autoantibodies Biomarkers CLINICAL NEUROLOGY Double-Blind Method Function and Dysfunction of the Nervous System General Neurology Humans Immunoglobulin G Integrative Biomedicine [Topic 3] Intermediate Filaments Mann-Whitney U test Monoclonal antibodies Neurology Neuromyelitis Optica Neuromyelitis Optica - blood Neuromyelitis Optica - drug therapy Proteins RANDOMISED TRIALS Statistical significance |
| Title | Serum neurofilament light chain levels at attack predict post-attack disability worsening and are mitigated by inebilizumab: analysis of four potential biomarkers in neuromyelitis optica spectrum disorder |
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