Ratio and index of Neurofilament light chain indicate its origin in Guillain-Barré Syndrome.
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Körtvelyessy P
German Center for Neurodegenerative Diseases (DZNE), Magdeburg, Germany.
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Kuhle J
Departments of Medicine, Biomedicine, and Clinical Research, Neurologic Clinic and Policlinic, University Hospital Basel, University of Basel, Basel, Switzerland.
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Düzel E
German Center for Neurodegenerative Diseases (DZNE), Magdeburg, Germany.
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Vielhaber S
Department of Neurology, University Hospital Magdeburg, Magdeburg, Germany.
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Schmidt C
Institute for Pharmacology, University Hospital Magdeburg, Magdeburg, Germany.
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Heinius A
Department of Neurology, Christian-Albrechts-University, University Hospital Schleswig-Holstein, Kiel, Germany.
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Leypoldt F
Department of Neurology, Christian-Albrechts-University, University Hospital Schleswig-Holstein, Kiel, Germany.
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Schraven B
Institute of Molecular and Clinical Immunology, Otto-von-Guericke-University Magdeburg, Magdeburg, Germany.
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Reinhold D
Institute of Molecular and Clinical Immunology, Otto-von-Guericke-University Magdeburg, Magdeburg, Germany.
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Leppert D
Departments of Medicine, Biomedicine, and Clinical Research, Neurologic Clinic and Policlinic, University Hospital Basel, University of Basel, Basel, Switzerland.
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Goihl A
Institute of Molecular and Clinical Immunology, Otto-von-Guericke-University Magdeburg, Magdeburg, Germany.
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Published in:
- Annals of clinical and translational neurology. - 2020
English
OBJECTIVE
Neurofilament light chain (NfL) has been established as a biomarker of axonal damage in many diseases of the central nervous system (CNS). Increased levels of serum NfL (sNfL) can derive as well from damage in the peripheral nervous system (PNS) as from CNS, but little is known about the quantities contributing to sNfL. Peripheral nerve damage may be reflected by an increase in sNfL levels, while the NfL CSF/serum ratio and NfL index decreases.
METHODS
We collected serum and cerebrospinal fluid (CSF) from 21 Guillain-Barré Syndrome (GBS) patients and measured NfL in serum and CSF and compared them with 19 neurologically healthy controls.
RESULTS
In general, NfL in CSF and serum was significantly higher in GBS patients. Serum NfL was higher in GBS patients admitted to the intensive care unit (P = 0.02). Controls had a mean CSF/serum NfL ratio of 26.7 (ranging from 5.8 to 69.5) indicating a central origin of NfL. Three GBS patients had a similar range (23.9 to 42.7, mean 33.3) all of them with demyelinating pathology in the PNS. Eighteen GBS patients with axonal or mixed axonal-demyelinating pathology showed significantly lower CSF/serum ratios (0.02-12.2, mean 4.4), indicative of a peripheral origin of NfL. When applying the NfL index subdivisions remain the same.
INTERPRETATION
These results demonstrate that the PNS is a relevant contributor to sNfL levels and that the distribution can be identified by a lowered NfL CSF/serum ratio of NfL index. Furthermore, acute or subacute polyneuropathies are likely confounding factors in interpreting sNfL levels in CNS diseases.
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Language
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Open access status
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gold
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Identifiers
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Persistent URL
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https://sonar.ch/global/documents/290491
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