Neurofilament light in plasma is a potential biomarker of central nervous system involvement in systemic lupus erythematosus.


Journal

Journal of neurology
ISSN: 1432-1459
Titre abrégé: J Neurol
Pays: Germany
ID NLM: 0423161

Informations de publication

Date de publication:
Jun 2022
Historique:
received: 09 09 2021
accepted: 05 11 2021
revised: 04 11 2021
pubmed: 21 11 2021
medline: 24 5 2022
entrez: 20 11 2021
Statut: ppublish

Résumé

Neuropsychiatric manifestations (NP) are common in systemic lupus erythematosus (SLE). However, the pathophysiological mechanisms are not completely understood. Neurofilament light protein (NfL) is part of the neuronal cytoskeleton. Increased NfL concentrations, reflecting neurodegeneration, is observed in cerebrospinal fluid (CSF) in several neurodegenerative and neuroinflammatory conditions. We aimed to explore if plasma NfL could serve as a biomarker for central nervous system (CNS) involvement in SLE. Sixty-seven patients with SLE underwent neurological examination; 52 underwent lumbar puncture, while 62 underwent cerebral magnetic resonance imaging (MRI). We measured selected auto-antibodies and other laboratory variables postulated to have roles in NP pathophysiology in the blood and/or CSF. We used SPM12 software for MRI voxel-based morphometry. Age-adjusted linear regression analyses revealed increased plasma NfL concentrations with increasing creatinine (β = 0.01, p < 0.001) and Q-albumin (β = 0.07, p = 0.008). We observed higher plasma NfL concentrations in patients with a history of seizures (β = 0.57, p = 0.014), impaired motor function (β = 0.36, p = 0.008), increasing disease activity (β = 0.04, p = 0.008), and organ damage (β = 0.10, p = 0.002). Voxel-based morphometry suggested an association between increasing plasma NfL concentrations and the loss of cerebral white matter in the corpus callosum and hippocampal gray matter. Increased plasma NfL concentrations were associated with some abnormal neurological, cognitive, and neuroimaging findings. However, plasma NfL was also influenced by other factors, such as damage accrual, creatinine, and Q-albumin, thereby obscuring the interpretation of how plasma NfL reflects CNS involvement. Taken together, NfL in CSF seems a better marker of neuronal injury than plasma NfL in patients with SLE.

Sections du résumé

BACKGROUND BACKGROUND
Neuropsychiatric manifestations (NP) are common in systemic lupus erythematosus (SLE). However, the pathophysiological mechanisms are not completely understood. Neurofilament light protein (NfL) is part of the neuronal cytoskeleton. Increased NfL concentrations, reflecting neurodegeneration, is observed in cerebrospinal fluid (CSF) in several neurodegenerative and neuroinflammatory conditions. We aimed to explore if plasma NfL could serve as a biomarker for central nervous system (CNS) involvement in SLE.
METHODS METHODS
Sixty-seven patients with SLE underwent neurological examination; 52 underwent lumbar puncture, while 62 underwent cerebral magnetic resonance imaging (MRI). We measured selected auto-antibodies and other laboratory variables postulated to have roles in NP pathophysiology in the blood and/or CSF. We used SPM12 software for MRI voxel-based morphometry.
RESULTS RESULTS
Age-adjusted linear regression analyses revealed increased plasma NfL concentrations with increasing creatinine (β = 0.01, p < 0.001) and Q-albumin (β = 0.07, p = 0.008). We observed higher plasma NfL concentrations in patients with a history of seizures (β = 0.57, p = 0.014), impaired motor function (β = 0.36, p = 0.008), increasing disease activity (β = 0.04, p = 0.008), and organ damage (β = 0.10, p = 0.002). Voxel-based morphometry suggested an association between increasing plasma NfL concentrations and the loss of cerebral white matter in the corpus callosum and hippocampal gray matter.
CONCLUSION CONCLUSIONS
Increased plasma NfL concentrations were associated with some abnormal neurological, cognitive, and neuroimaging findings. However, plasma NfL was also influenced by other factors, such as damage accrual, creatinine, and Q-albumin, thereby obscuring the interpretation of how plasma NfL reflects CNS involvement. Taken together, NfL in CSF seems a better marker of neuronal injury than plasma NfL in patients with SLE.

Identifiants

pubmed: 34800169
doi: 10.1007/s00415-021-10893-z
pii: 10.1007/s00415-021-10893-z
doi:

Substances chimiques

Albumins 0
Biomarkers 0
Neurofilament Proteins 0
neurofilament protein L 0
Creatinine AYI8EX34EU

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

3064-3074

Subventions

Organisme : Helse Vest
ID : F-12525
Organisme : Helse Vest
ID : 912129
Organisme : Helse Vest
ID : 911807
Organisme : Vetenskapsrådet
ID : 2018-02532
Organisme : Vetenskapsrådet
ID : 2017-00915
Organisme : H2020 European Research Council
ID : 681712
Organisme : Swedish State Support for Clinical Research
ID : ALFGBG-720931
Organisme : Alzheimer's Drug Discovery Foundation
ID : 201809-2016862
Organisme : The Swedish Alzheimer's Foundation
ID : AF-742881
Organisme : Hjärnfonden
ID : FO2017-0243
Organisme : the European Union Joint Program for Neurodegenerative Disorders
ID : JPND2019-466-236
Organisme : Norges Forskningsråd
ID : 287842
Organisme : Japan Agency for Medical Research and Development
ID : 15eK0410022h0001

Informations de copyright

© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany.

Références

Hanly JG, Kozora E, Beyea SD, Birnbaum J (2019) Review: nervous system disease in systemic lupus erythematosus: current status and future directions. Arthritis Rheumatol (Hoboken, NJ) 71(1):33–42. https://doi.org/10.1002/art.40591
doi: 10.1002/art.40591
Faust TW, Chang EH, Kowal C, Berlin R, Gazaryan IG, Bertini E, Zhang J, Sanchez-Guerrero J, Fragoso-Loyo HE, Volpe BT, Diamond B, Huerta PT (2010) Neurotoxic lupus autoantibodies alter brain function through two distinct mechanisms. Proc Natl Acad Sci USA 107(43):18569–18574. https://doi.org/10.1073/pnas.1006980107
doi: 10.1073/pnas.1006980107 pubmed: 20921396 pmcid: 2972998
Gaetani L, Blennow K, Calabresi P, Di Filippo M, Parnetti L, Zetterberg H (2019) Neurofilament light chain as a biomarker in neurological disorders. J Neurol Neurosurg Psychiatry 90(8):870–881. https://doi.org/10.1136/jnnp-2018-320106
doi: 10.1136/jnnp-2018-320106 pubmed: 30967444
Tjensvoll AB, Lauvsnes MB, Zetterberg H, Kvaloy JT, Kvivik I, Maroni SS, Greve OJ, Beyer MK, Hirohata S, Putterman C, Alves G, Harboe E, Blennow K, Goransson LG, Omdal R (2021) Neurofilament light is a biomarker of brain involvement in lupus and primary Sjogren’s syndrome. J Neurol 268(4):1385–1394. https://doi.org/10.1007/s00415-020-10290-y
doi: 10.1007/s00415-020-10290-y pubmed: 33128084
Mielke MM, Syrjanen JA, Blennow K, Zetterberg H, Vemuri P, Skoog I, Machulda MM, Kremers WK, Knopman DS, Jack C Jr, Petersen RC, Kern S (2019) Plasma and CSF neurofilament light: relation to longitudinal neuroimaging and cognitive measures. Neurology 93(3):e252–e260. https://doi.org/10.1212/WNL.0000000000007767
doi: 10.1212/WNL.0000000000007767 pubmed: 31182505 pmcid: 6656645
Appenzeller S, Carnevalle AD, Li LM, Costallat LT, Cendes F (2006) Hippocampal atrophy in systemic lupus erythematosus. Ann Rheum Dis 65(12):1585–1589. https://doi.org/10.1136/ard.2005.049486
doi: 10.1136/ard.2005.049486 pubmed: 16439436 pmcid: 1798450
Appenzeller S, Rondina JM, Li LM, Costallat LT, Cendes F (2005) Cerebral and corpus callosum atrophy in systemic lupus erythematosus. Arthritis Rheum 52(9):2783–2789. https://doi.org/10.1002/art.21271
doi: 10.1002/art.21271 pubmed: 16142703
Akamine S, Marutani N, Kanayama D, Gotoh S, Maruyama R, Yanagida K, Sakagami Y, Mori K, Adachi H, Kozawa J, Maeda N, Otsuki M, Matsuoka T, Iwahashi H, Shimomura I, Ikeda M, Kudo T (2020) Renal function is associated with blood neurofilament light chain level in older adults. Sci Rep 10(1):20350. https://doi.org/10.1038/s41598-020-76990-7
doi: 10.1038/s41598-020-76990-7 pubmed: 33230211 pmcid: 7683708
Hochberg MC (1997) Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum 40(9):1725. https://doi.org/10.1002/1529-0131(199709)40:9%3c1725::AID-ART29%3e3.0.CO;2-Y
doi: 10.1002/1529-0131(199709)40:9<1725::AID-ART29>3.0.CO;2-Y pubmed: 9324032
Wechsler D (1955) Manual for the Wechsler Adult Intelligence Scale. Manual for the Wechsler Adult Intelligence Scale. Psychological Corp., Oxford
Wechsler D (1987) WMS-R: Wechsler Memory Scale-revised: manual. Harcourt Brace Jovanovich, New York
Heaton RK, Chelune GJ, Talley JL, Kay GG, Curtiss G (1993) Wisconsin card sorting test manual: revised and expanded. Psychological Assessment Resources Inc, Odessa
Stroop JR (1935) Studies of interference in serial verbal reactions. J Exp Psychol 18:643–662
doi: 10.1037/h0054651
Reitan RM, Wolfson D (1985) The Halstead-Reitan neuropsychological test battery: theory and clinical interpretation. Neuropsychology Press, Tucson
ACR Ad Hoc Committee on Neuropsychiatric Lupus Nomenclature (1999) The American College of Rheumatology nomenclature and case definitions for neuropsychiatric lupus syndromes. Arthritis Rheum 42(4):599–608. https://doi.org/10.1002/1529-0131(199904)42:4%3c599::AID-ANR2%3e3.0.CO;2-F
doi: 10.1002/1529-0131(199904)42:4<599::AID-ANR2>3.0.CO;2-F
Tibbling G, Link H, Ohman S (1977) Principles of albumin and IgG analyses in neurological disorders. I. Establishment of reference values. Scand J Clin Lab Investig 37(5):385–390. https://doi.org/10.1080/00365517709091496
doi: 10.1080/00365517709091496
Harboe E, Tjensvoll AB, Maroni S, Goransson LG, Greve OJ, Beyer MK, Herigstad A, Kvaloy JT, Omdal R (2009) Neuropsychiatric syndromes in patients with systemic lupus erythematosus and primary Sjogren syndrome: a comparative population-based study. Ann Rheum Dis 68(10):1541–1546. https://doi.org/10.1136/ard.2008.098301
doi: 10.1136/ard.2008.098301 pubmed: 18930990
Lauvsnes MB, Maroni SS, Appenzeller S, Beyer MK, Greve OJ, Kvaloy JT, Harboe E, Goransson LG, Tjensvoll AB, Omdal R (2013) Memory dysfunction in primary Sjogren’s syndrome is associated with anti-NR2 antibodies. Arthritis Rheum 65(12):3209–3217. https://doi.org/10.1002/art.38127
doi: 10.1002/art.38127 pubmed: 23982950
Isshi K, Hirohata S (1996) Association of anti-ribosomal P protein antibodies with neuropsychiatric systemic lupus erythematosus. Arthritis Rheum 39(9):1483–1490
doi: 10.1002/art.1780390907
Harboe E, Beyer MK, Greve OJ, Goransson LG, Tjensvoll AB, Kvaloy JT, Omdal R (2009) Cerebral white matter hyperintensities are not increased in patients with primary Sjogren’s syndrome. Eur J Neurol 16(5):576–581. https://doi.org/10.1111/j.1468-1331.2009.02537.x
doi: 10.1111/j.1468-1331.2009.02537.x pubmed: 19220446
Lauvsnes MB, Beyer MK, Kvaloy JT, Greve OJ, Appenzeller S, Kvivik I, Harboe E, Tjensvoll AB, Goransson LG, Omdal R (2014) Association of hippocampal atrophy with cerebrospinal fluid antibodies against the NR2 subtype of the N-methyl-D-aspartate receptor in patients with systemic lupus erythematosus and patients with primary Sjogren’s syndrome. Arthritis Rheumatol (Hoboken, NJ) 66(12):3387–3394. https://doi.org/10.1002/art.38852
doi: 10.1002/art.38852
Ashburner J, Friston KJ (2000) Voxel-based morphometry–the methods. Neuroimage 11(6 Pt 1):805–821. https://doi.org/10.1006/nimg.2000.0582
doi: 10.1006/nimg.2000.0582 pubmed: 10860804
Maldjian JA, Laurienti PJ, Kraft RA, Burdette JH (2003) An automated method for neuroanatomic and cytoarchitectonic atlas-based interrogation of fMRI data sets. Neuroimage 19(3):1233–1239
doi: 10.1016/S1053-8119(03)00169-1
Maldjian JA, Laurienti PJ, Burdette JH (2004) Precentral gyrus discrepancy in electronic versions of the Talairach atlas. Neuroimage 21(1):450–455
doi: 10.1016/j.neuroimage.2003.09.032
Friston KJ, Worsley KJ, Frackowiak RSJ, Mazziotta JC, Evans AC (1993) Assessing the significance of focal activations using their spatial extent. Hum Brain Mapp 1(3):210–220. https://doi.org/10.1002/hbm.460010306
doi: 10.1002/hbm.460010306
Serbruyns L, Gooijers J, Caeyenberghs K, Meesen RL, Cuypers K, Sisti HM, Leemans A, Swinnen SP (2015) Bimanual motor deficits in older adults predicted by diffusion tensor imaging metrics of corpus callosum subregions. Brain Struct Funct 220(1):273–290. https://doi.org/10.1007/s00429-013-0654-z
doi: 10.1007/s00429-013-0654-z pubmed: 24158531
Pujol-Calderon F, Portelius E, Zetterberg H, Blennow K, Rosengren LE, Hoglund K (2019) Neurofilament changes in serum and cerebrospinal fluid after acute ischemic stroke. Neurosci Lett 698:58–63. https://doi.org/10.1016/j.neulet.2018.12.042
doi: 10.1016/j.neulet.2018.12.042 pubmed: 30599262
Ainiala H, Loukkola J, Peltola J, Korpela M, Hietaharju A (2001) The prevalence of neuropsychiatric syndromes in systemic lupus erythematosus. Neurology 57(3):496–500
doi: 10.1212/WNL.57.3.496

Auteurs

Maria Boge Lauvsnes (MB)

Department of Rheumatology, Stavanger University Hospital, Pb. 8100 Forus, 4068, Stavanger, Norway. mariaboge@hotmail.com.

Henrik Zetterberg (H)

Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
UK Dementia Research Institute at UCL, London, UK.
Department of Neurodegenerative Disease, UCL Institute of Neurology, London, UK.

Kaj Blennow (K)

Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.

Jan Terje Kvaløy (JT)

Research Department, Stavanger University Hospital, Stavanger, Norway.
Department of Mathematics and Physics, Bioscience and Environmental Engineering, University of Stavanger, Stavanger, Norway.

Anne Bolette Tjensvoll (AB)

Department of Neurology, Stavanger University Hospital, Stavanger, Norway.

Stian Maroni (S)

Clinical Neuropsychology Unit, Division of Psychiatry, Stavanger University Hospital, Stavanger, Norway.

Mona K Beyer (MK)

Instiute of Clinical Medicine, University of Oslo, Oslo, Norway.
Division of Radiology and Nuclear Medicine, Oslo University Hospital, Oslo, Norway.

Ole Jacob Greve (OJ)

Department of Radiology, Stavanger University Hospital, Stavanger, Norway.

Ingeborg Kvivik (I)

Research Department, Stavanger University Hospital, Stavanger, Norway.

Guido Alves (G)

Department of Neurology, Stavanger University Hospital, Stavanger, Norway.
The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway.
Department of Chemistry, Bioscience and Environmental Engineering, University of Stavanger, Stavanger, Norway.

Lasse Gunnar Gøransson (LG)

Department of Internal Medicine, Stavanger University Hospital, Stavanger, Norway.
Department of Clinical Science, Faculty of Medicine, University of Bergen, Bergen, Norway.

Erna Harboe (E)

Department of Internal Medicine, Stavanger University Hospital, Stavanger, Norway.

Shunsei Hirohata (S)

Department of Rheumatology and Infectious Diseases, Kitasato University School of Medicine, Sagamihara, Japan.

Roald Omdal (R)

Department of Rheumatology, Stavanger University Hospital, Pb. 8100 Forus, 4068, Stavanger, Norway.
Department of Clinical Science, Faculty of Medicine, University of Bergen, Bergen, Norway.

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