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September 13, 2016; 87 (11) Editorial

CSF neurofilament light

A universal risk biomarker in multiple sclerosis?

Michael Khalil, Jonatan Salzer
First published August 12, 2016, DOI: https://doi.org/10.1212/WNL.0000000000003107
Michael Khalil
From the Department of Neurology (M.K.), Medical University of Graz, Austria; and Department of Neurology (J.S.), Umeå University Hospital, Sweden.
MD, PhD
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Jonatan Salzer
From the Department of Neurology (M.K.), Medical University of Graz, Austria; and Department of Neurology (J.S.), Umeå University Hospital, Sweden.
MD, PhD
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Citation
CSF neurofilament light
A universal risk biomarker in multiple sclerosis?
Michael Khalil, Jonatan Salzer
Neurology Sep 2016, 87 (11) 1068-1069; DOI: 10.1212/WNL.0000000000003107

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Axonal loss from relapses and neurodegeneration is a main element of multiple sclerosis (MS) pathology, so an objective biomarker to detect and quantify it should be of great value. Neurofilaments belong to the intermediate filament family of proteins and are the major components of the cytoskeleton of neurons. They consist of 3 isotypes: a neurofilament light (NfL) chain of 68 kDa, a neurofilament intermediate (NfM) chain of 150 kDa, and a neurofilament heavy (NfH) chain of 190 to 210 kDa.1 During the process of axonal injury, intracellular components, including neurofilaments, are released into the extracellular fluid and subsequently into the CSF. Thus, analysis of neurofilament levels in the CSF may reliably capture the extent of axonal damage and neurodegeneration in the CNS, regardless of the underlying cause.1 Evidence for increased CSF neurofilament levels in MS mainly exists for NfH and NfL, whereas NfM has not been extensively studied so far.1 Several test systems exist to determine NfH and NfL, and a commercially available ELISA to detect NfL is advantageous in discriminating patients with MS from controls.2

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  • Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the editorial.

  • See page 1076

  • © 2016 American Academy of Neurology
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