Evidence map›Paper›PMID 30171200›Full record

ReviewNature reviews. Neurology2018

Neurofilaments as biomarkers in neurological disorders.

Michael Khalil, Charlotte E Teunissen, Markus Otto, Fredrik Piehl, Maria Pia Sormani, Thomas Gattringer, Christian Barro, Ludwig Kappos, Manuel Comabella, Franz Fazekas and 4 more

3 registry-linked trialsOpen access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 3 registered trials, which are not on this map. Cited by 1,170 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,170citing papers in PubMed, 7 pooled it
104.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT04674163 nawithdrawnnot on this mapstarted 2023, after this paper: background citation

NEUROKINASE : Expression Profile of ERK5 and PKM2 Kinases in Neuroinflammatory Diseases.

TypeinterventionalSponsorCentre Hospitalier Régional d'OrléansRan2023 to 2023Enrolled0ConditionsSclerosis, Multiple, Guillain-Barre Syndrome, InflammationArmsBlood sample and Cerebrospinal fluid (CSF) collection.
NCT05821816 nacompletednot on this mapstarted 2023, after this paper: background citation

Evaluation of the Efficacy of Transcranial Direct Current Stimulation (tDCS) on Neurodegeneration and Neuromotor Recovery on Post-stroke Patients. a Pilot Study

TypeinterventionalSponsorI.R.C.C.S. Fondazione Santa LuciaRan2023 to 2025Enrolled50ConditionsStrokeArmstDCS, Conventional rehabilitative treatment
NCT05911139 enrolling by invitationnot on this mapstarted 2022, after this paper: background citation

Influence of General Anesthesia on the Dynamic Changes in Brain Damage Markers During and After Craniosynostosis Operations in Infancy

Typeobservational_patient_registrySponsorComenius UniversityRan2022 to 2026Enrolled45ConditionsCraniosynostosis, Anesthesia
3 · Its place in the literature

Who cites it

1,170 citing papers in PubMed, 7 syntheses or guidelines pooled it, 1,887 citations in OpenAlex.

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  16. Nutritional state-dependent changes in subcortical limbic structures in anorexia nervosa are linked to leptin, ghrelin, and neurofilament light.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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1,110 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 8 institutions in 8 countries.

Michael KhalilDepartment of Neurology, Medical University of Graz, Graz, Austria. michael.khalil@medunigraz.at.ORCID http://orcid.org/0000-0002-5350-3328
Charlotte E TeunissenNeurochemistry Laboratory and Biobank, Department of Clinical Chemistry, Amsterdam Neuroscience, Amsterdam University Medical Centers, Amsterdam, Netherlands.
Markus OttoDepartment of Neurology, Ulm University Hospital, Ulm, Germany.ORCID http://orcid.org/0000-0003-4273-4267
Fredrik PiehlDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Maria Pia SormaniDepartment of Health Sciences, University of Genoa, Genoa, Italy.
Thomas GattringerDepartment of Neurology, Medical University of Graz, Graz, Austria.
Christian BarroNeurologic Clinic and Policlinic, Departments of Medicine, Clinical Research, and Biomedicine, University Hospital Basel, University of Basel, Basel, Switzerland.
Ludwig KapposNeurologic Clinic and Policlinic, Departments of Medicine, Clinical Research, and Biomedicine, University Hospital Basel, University of Basel, Basel, Switzerland.
Manuel ComabellaUnit of Clinical Neuroimmunology, Department of Neurology, Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain.
Franz FazekasDepartment of Neurology, Medical University of Graz, Graz, Austria.ORCID http://orcid.org/0000-0001-8155-7799
Axel PetzoldUCL Institute of Neurology, Department of Molecular Neurosciences, Moorfields Eye Hospital and The National Hospital for Neurology and Neurosurgery, London, UK.ORCID http://orcid.org/0000-0002-0344-9749
Kaj BlennowClinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Henrik ZetterbergClinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Jens KuhleNeurologic Clinic and Policlinic, Departments of Medicine, Clinical Research, and Biomedicine, University Hospital Basel, University of Basel, Basel, Switzerland. jens.kuhle@usb.ch.
Medical University of Graz · ATUniversity of Basel · CHAmsterdam Neuroscience · NLSahlgrenska University Hospital · SEKarolinska Institutet · SEOspedale Policlinico San Martino · ITUniversitat Autònoma de Barcelona · ESUniversity Hospital Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AgingAmyotrophic Lateral SclerosisBiomarkersBipolar DisorderBrain Injuries, TraumaticDementiaHumansHuntington DiseaseImmunoassayMultiple SclerosisNeurofilament ProteinsParkinson DiseaseStrokeBiomarkersNeurofilament Proteins

Identifiers

PMID30171200
OpenAlexW2889223700

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.