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Nat Rev Neurol. 2018 Oct;14(10):577-589. doi: 10.1038/s41582-018-0058-z.

Neurofilaments as biomarkers in neurological disorders.

Author information

1
Department of Neurology, Medical University of Graz, Graz, Austria. michael.khalil@medunigraz.at.
2
Neurochemistry Laboratory and Biobank, Department of Clinical Chemistry, Amsterdam Neuroscience, Amsterdam University Medical Centers, Amsterdam, Netherlands.
3
Department of Neurology, Ulm University Hospital, Ulm, Germany.
4
Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
5
Department of Health Sciences, University of Genoa, Genoa, Italy.
6
Ospedale Policlinico San Martino IRCCS, Genoa, Italy.
7
Department of Neurology, Medical University of Graz, Graz, Austria.
8
Neurologic Clinic and Policlinic, Departments of Medicine, Clinical Research, and Biomedicine, University Hospital Basel, University of Basel, Basel, Switzerland.
9
Unit of Clinical Neuroimmunology, Department of Neurology, Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain.
10
UCL Institute of Neurology, Department of Molecular Neurosciences, Moorfields Eye Hospital and The National Hospital for Neurology and Neurosurgery, London, UK.
11
Departments of Neurology, Ophthalmology and Expertise Center for Neuro-ophthalmology, Amsterdam UMC, Amsterdam, Netherlands.
12
Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
13
Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden.
14
Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London, UK.
15
UK Dementia Research Institute at UCL, London, UK.
16
Neurologic Clinic and Policlinic, Departments of Medicine, Clinical Research, and Biomedicine, University Hospital Basel, University of Basel, Basel, Switzerland. jens.kuhle@usb.ch.

Abstract

Neuroaxonal damage is the pathological substrate of permanent disability in various neurological disorders. Reliable quantification and longitudinal follow-up of such damage are important for assessing disease activity, monitoring treatment responses, facilitating treatment development and determining prognosis. The neurofilament proteins have promise in this context because their levels rise upon neuroaxonal damage not only in the cerebrospinal fluid (CSF) but also in blood, and they indicate neuroaxonal injury independent of causal pathways. First-generation (immunoblot) and second-generation (enzyme-linked immunosorbent assay) neurofilament assays had limited sensitivity. Third-generation (electrochemiluminescence) and particularly fourth-generation (single-molecule array) assays enable the reliable measurement of neurofilaments throughout the range of concentrations found in blood samples. This technological advancement has paved the way to investigate neurofilaments in a range of neurological disorders. Here, we review what is known about the structure and function of neurofilaments, discuss analytical aspects and knowledge of age-dependent normal ranges of neurofilaments and provide a comprehensive overview of studies on neurofilament light chain as a marker of axonal injury in different neurological disorders, including multiple sclerosis, neurodegenerative dementia, stroke, traumatic brain injury, amyotrophic lateral sclerosis and Parkinson disease. We also consider work needed to explore the value of this axonal damage marker in managing neurological diseases in daily practice.

PMID:
30171200
DOI:
10.1038/s41582-018-0058-z
[Indexed for MEDLINE]

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