Neurofilaments as biomarkers in neurological disorders

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 determini...

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Veröffentlicht in:	Nature reviews. Neurology Jg. 14; H. 10; S. 577 - 589
Hauptverfasser:	Khalil, Michael, Teunissen, Charlotte E, Otto, Markus, Piehl, Fredrik, Sormani, Maria Pia, Gattringer, Thomas, Barro, Christian, Kappos, Ludwig, Comabella, Manuel, Fazekas, Franz, Petzold, Axel, Blennow, Kaj, Zetterberg, Henrik, Kuhle, Jens
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	England Nature Publishing Group 01.10.2018
Schlagworte:	Aging - metabolism Amyotrophic Lateral Sclerosis - diagnosis Amyotrophic Lateral Sclerosis - metabolism Biomarkers Biomarkers - metabolism Bipolar Disorder - diagnosis Bipolar Disorder - metabolism Brain Injuries, Traumatic - diagnosis Brain Injuries, Traumatic - metabolism Dementia - diagnosis Dementia - metabolism Disease Enzymes Humans Huntington Disease - diagnosis Huntington Disease - metabolism Immunoassay - methods Multiple Sclerosis - diagnosis Multiple Sclerosis - metabolism Neurofilament Proteins - blood Neurofilament Proteins - cerebrospinal fluid Neurofilament Proteins - metabolism Neurological disorders Parkinson Disease - diagnosis Parkinson Disease - metabolism Parkinson's disease Stroke - diagnosis Stroke - metabolism
ISSN:	1759-4758, 1759-4766, 1759-4766
Online-Zugang:	Volltext
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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.
AbstractList	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. 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.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. 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.
Author	Sormani, Maria Pia Fazekas, Franz Petzold, Axel Kuhle, Jens Teunissen, Charlotte E Zetterberg, Henrik Gattringer, Thomas Otto, Markus Comabella, Manuel Piehl, Fredrik Kappos, Ludwig Khalil, Michael Barro, Christian Blennow, Kaj
Author_xml	– sequence: 1 givenname: Michael orcidid: 0000-0002-5350-3328 surname: Khalil fullname: Khalil, Michael email: michael.khalil@medunigraz.at organization: Department of Neurology, Medical University of Graz, Graz, Austria. michael.khalil@medunigraz.at – sequence: 2 givenname: Charlotte E surname: Teunissen fullname: Teunissen, Charlotte E organization: Neurochemistry Laboratory and Biobank, Department of Clinical Chemistry, Amsterdam Neuroscience, Amsterdam University Medical Centers, Amsterdam, Netherlands – sequence: 3 givenname: Markus orcidid: 0000-0003-4273-4267 surname: Otto fullname: Otto, Markus organization: Department of Neurology, Ulm University Hospital, Ulm, Germany – sequence: 4 givenname: Fredrik surname: Piehl fullname: Piehl, Fredrik organization: Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden – sequence: 5 givenname: Maria Pia surname: Sormani fullname: Sormani, Maria Pia organization: Ospedale Policlinico San Martino IRCCS, Genoa, Italy – sequence: 6 givenname: Thomas surname: Gattringer fullname: Gattringer, Thomas organization: Department of Neurology, Medical University of Graz, Graz, Austria – sequence: 7 givenname: Christian surname: Barro fullname: Barro, Christian organization: Neurologic Clinic and Policlinic, Departments of Medicine, Clinical Research, and Biomedicine, University Hospital Basel, University of Basel, Basel, Switzerland – sequence: 8 givenname: Ludwig surname: Kappos fullname: Kappos, Ludwig organization: Neurologic Clinic and Policlinic, Departments of Medicine, Clinical Research, and Biomedicine, University Hospital Basel, University of Basel, Basel, Switzerland – sequence: 9 givenname: Manuel surname: Comabella fullname: Comabella, Manuel organization: Unit of Clinical Neuroimmunology, Department of Neurology, Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain – sequence: 10 givenname: Franz orcidid: 0000-0001-8155-7799 surname: Fazekas fullname: Fazekas, Franz organization: Department of Neurology, Medical University of Graz, Graz, Austria – sequence: 11 givenname: Axel orcidid: 0000-0002-0344-9749 surname: Petzold fullname: Petzold, Axel organization: Departments of Neurology, Ophthalmology and Expertise Center for Neuro-ophthalmology, Amsterdam UMC, Amsterdam, Netherlands – sequence: 12 givenname: Kaj surname: Blennow fullname: Blennow, Kaj organization: Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden – sequence: 13 givenname: Henrik surname: Zetterberg fullname: Zetterberg, Henrik organization: UK Dementia Research Institute at UCL, London, UK – sequence: 14 givenname: Jens surname: Kuhle fullname: Kuhle, Jens email: jens.kuhle@usb.ch organization: Neurologic Clinic and Policlinic, Departments of Medicine, Clinical Research, and Biomedicine, University Hospital Basel, University of Basel, Basel, Switzerland. jens.kuhle@usb.ch
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/30171200$$D View this record in MEDLINE/PubMed
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Snippet	Neuroaxonal damage is the pathological substrate of permanent disability in various neurological disorders. Reliable quantification and longitudinal follow-up...
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SubjectTerms	Aging - metabolism Amyotrophic Lateral Sclerosis - diagnosis Amyotrophic Lateral Sclerosis - metabolism Biomarkers Biomarkers - metabolism Bipolar Disorder - diagnosis Bipolar Disorder - metabolism Brain Injuries, Traumatic - diagnosis Brain Injuries, Traumatic - metabolism Dementia - diagnosis Dementia - metabolism Disease Enzymes Humans Huntington Disease - diagnosis Huntington Disease - metabolism Immunoassay - methods Multiple Sclerosis - diagnosis Multiple Sclerosis - metabolism Neurofilament Proteins - blood Neurofilament Proteins - cerebrospinal fluid Neurofilament Proteins - metabolism Neurological disorders Parkinson Disease - diagnosis Parkinson Disease - metabolism Parkinson's disease Stroke - diagnosis Stroke - metabolism
Title	Neurofilaments as biomarkers in neurological disorders
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