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

Lauvsnes, M. B. (author)
Zetterberg, Henrik, 1973 (author)
Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Blennow, Kaj, 1958 (author)
Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
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Kvaloy, J. T. (author)
Tjensvoll, A. B. (author)
Maroni, S. (author)
Beyer, M. K. (author)
Greve, O. J. (author)
Kvivik, I. (author)
Alves, G. (author)
Goransson, L. G. (author)
Harboe, E. (author)
Hirohata, S. (author)
Omdal, R. (author)
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 (creator_code:org_t)
2021-11-20
2022
English.
In: Journal of Neurology. - : Springer Science and Business Media LLC. - 0340-5354 .- 1432-1459. ; 269, s. 3064-3074
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • 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 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 Age-adjusted linear regression analyses revealed increased plasma NfL concentrations with increasing creatinine (beta = 0.01, p < 0.001) and Q-albumin (beta = 0.07, p = 0.008). We observed higher plasma NfL concentrations in patients with a history of seizures (beta = 0.57, p = 0.014), impaired motor function (beta = 0.36, p = 0.008), increasing disease activity (beta = 0.04, p = 0.008), and organ damage (beta = 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 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.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Neurovetenskaper (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Neurosciences (hsv//eng)

Keyword

Systemic lupus erythematosus
Neurofilament light
Central nervous
system
Cerebral imaging
Biomarker
hippocampal atrophy
association
antibodies
Neurosciences & Neurology

Publication and Content Type

ref (subject category)
art (subject category)

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