ArticleNeurology2018
Neurofilament light protein in blood predicts regional atrophy in Huntington disease.
Open access · bronzeAbstract readMulticenter Study
In one paragraph
Article in Neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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47citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 4% of its field
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The trial behind it
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- Systematic Review with Meta-Analysis of Biofluid Markers for Huntington's Disease.Movement disorders : official journal of the Movement Disorder Society · 2025Pooled it
- Neurofilament light is a treatment-responsive biomarker in CLN2 disease.Annals of clinical and translational neurology · 2019Trial
- Neurofilament Light Chain (NfL) in Neurodegenerative Diseases: Biological and Clinical Significance, Multi-Omics Integration, and AI-Driven Biomarker Modeling for Precision Therapy.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Article
- Quantifying brain-age gap in people with HIV on antiretroviral therapy using plasma neurofilament light chain.AIDS (London, England) · 2026Article
- Profiles of patients at early stages of Huntington's disease based on the routine biological markers and the disease progression.Journal of neurology · 2026Article
- Cerebrospinal Fluid Proenkephalin Predicts Striatal Atrophy Decades before Clinical Motor Diagnosis in Huntington's Disease.Movement disorders : official journal of the Movement Disorder Society · 2026Article
- The role of neurofilament light chain and other fluid biomarkers in cerebellar ataxias.Brain communications · 2026Review
- Molecular and imaging biomarker responses to brain mutant HTT lowering in a mouse model of Huntington disease.Molecular therapy. Nucleic acids · 2025Article
- Article
- Advances in Huntington's Disease Biomarkers: A 10-Year Bibliometric Analysis and a Comprehensive Review.Biology · 2025Review
- A 14-year longitudinal study of neurofilament light chain dynamics in premanifest and transitional Huntington's disease.Journal of neurology · 2024Article
- Emerging Trends: Neurofilament Biomarkers in Precision Neurology.Neurochemical research · 2024Review
- Elevated plasma and CSF neurofilament light chain concentrations are stabilized in response to mutant huntingtin lowering in the brains of Huntington's disease mice.Translational neurodegeneration · 2024Article
- Comparison of Serum Neurofilament Light Chain and Tau Protein Levels in Cases with Autism Spectrum Disorder and Their Healthy Siblings and Healthy Controls.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2024Article
- CMS121 Partially Attenuates Disease Progression in Mouse Models of Huntington's Disease.Molecular neurobiology · 2024Article
- Clinical biomarkers for Lewy body diseases.Cell & bioscience · 2023Review
- Blood levels of neurofilament light are associated with disease progression in a mouse model of spinocerebellar ataxia type 3.Disease models & mechanisms · 2023Article
- The updated development of blood-based biomarkers for Huntington's disease.Journal of neurology · 2023Review
- Peripheral Biomarkers in Manifest and Premanifest Huntington's Disease.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 3 countries.
Eileanoir B JohnsonFrom the Huntington's Disease Research Centre (E.B.J., L.M.B., S.G., F.B.R., S.J.T., R.I.S., E.J.W.), UCL Institute of Neurology, London, UK; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institut du Cerveau et de la Moelle épinière (A.D.), Sorbonne Universités, UPMC University Paris 06, UMRS 1127, INSERM, U 1127, CNRS, UMR 7225; APHP (A.D.), Genetics Department, Pitié-Salpêtrière University Hospital, Paris, France; Centre for Molecular Medicine and Therapeutics (B.R.L.), University of British Columbia, Vancouver, BC, Canada; Department of Neurology (R.A.R.), Leiden University, the Netherlands; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; and UK Dementia Research Institute (H.Z.), London, UK.
Lauren M ByrneFrom the Huntington's Disease Research Centre (E.B.J., L.M.B., S.G., F.B.R., S.J.T., R.I.S., E.J.W.), UCL Institute of Neurology, London, UK; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institut du Cerveau et de la Moelle épinière (A.D.), Sorbonne Universités, UPMC University Paris 06, UMRS 1127, INSERM, U 1127, CNRS, UMR 7225; APHP (A.D.), Genetics Department, Pitié-Salpêtrière University Hospital, Paris, France; Centre for Molecular Medicine and Therapeutics (B.R.L.), University of British Columbia, Vancouver, BC, Canada; Department of Neurology (R.A.R.), Leiden University, the Netherlands; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; and UK Dementia Research Institute (H.Z.), London, UK.
Sarah GregoryFrom the Huntington's Disease Research Centre (E.B.J., L.M.B., S.G., F.B.R., S.J.T., R.I.S., E.J.W.), UCL Institute of Neurology, London, UK; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institut du Cerveau et de la Moelle épinière (A.D.), Sorbonne Universités, UPMC University Paris 06, UMRS 1127, INSERM, U 1127, CNRS, UMR 7225; APHP (A.D.), Genetics Department, Pitié-Salpêtrière University Hospital, Paris, France; Centre for Molecular Medicine and Therapeutics (B.R.L.), University of British Columbia, Vancouver, BC, Canada; Department of Neurology (R.A.R.), Leiden University, the Netherlands; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; and UK Dementia Research Institute (H.Z.), London, UK.
Filipe B RodriguesFrom the Huntington's Disease Research Centre (E.B.J., L.M.B., S.G., F.B.R., S.J.T., R.I.S., E.J.W.), UCL Institute of Neurology, London, UK; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institut du Cerveau et de la Moelle épinière (A.D.), Sorbonne Universités, UPMC University Paris 06, UMRS 1127, INSERM, U 1127, CNRS, UMR 7225; APHP (A.D.), Genetics Department, Pitié-Salpêtrière University Hospital, Paris, France; Centre for Molecular Medicine and Therapeutics (B.R.L.), University of British Columbia, Vancouver, BC, Canada; Department of Neurology (R.A.R.), Leiden University, the Netherlands; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; and UK Dementia Research Institute (H.Z.), London, UK.
Kaj BlennowFrom the Huntington's Disease Research Centre (E.B.J., L.M.B., S.G., F.B.R., S.J.T., R.I.S., E.J.W.), UCL Institute of Neurology, London, UK; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institut du Cerveau et de la Moelle épinière (A.D.), Sorbonne Universités, UPMC University Paris 06, UMRS 1127, INSERM, U 1127, CNRS, UMR 7225; APHP (A.D.), Genetics Department, Pitié-Salpêtrière University Hospital, Paris, France; Centre for Molecular Medicine and Therapeutics (B.R.L.), University of British Columbia, Vancouver, BC, Canada; Department of Neurology (R.A.R.), Leiden University, the Netherlands; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; and UK Dementia Research Institute (H.Z.), London, UK.
Alexandra DurrFrom the Huntington's Disease Research Centre (E.B.J., L.M.B., S.G., F.B.R., S.J.T., R.I.S., E.J.W.), UCL Institute of Neurology, London, UK; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institut du Cerveau et de la Moelle épinière (A.D.), Sorbonne Universités, UPMC University Paris 06, UMRS 1127, INSERM, U 1127, CNRS, UMR 7225; APHP (A.D.), Genetics Department, Pitié-Salpêtrière University Hospital, Paris, France; Centre for Molecular Medicine and Therapeutics (B.R.L.), University of British Columbia, Vancouver, BC, Canada; Department of Neurology (R.A.R.), Leiden University, the Netherlands; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; and UK Dementia Research Institute (H.Z.), London, UK.
Blair R LeavittFrom the Huntington's Disease Research Centre (E.B.J., L.M.B., S.G., F.B.R., S.J.T., R.I.S., E.J.W.), UCL Institute of Neurology, London, UK; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institut du Cerveau et de la Moelle épinière (A.D.), Sorbonne Universités, UPMC University Paris 06, UMRS 1127, INSERM, U 1127, CNRS, UMR 7225; APHP (A.D.), Genetics Department, Pitié-Salpêtrière University Hospital, Paris, France; Centre for Molecular Medicine and Therapeutics (B.R.L.), University of British Columbia, Vancouver, BC, Canada; Department of Neurology (R.A.R.), Leiden University, the Netherlands; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; and UK Dementia Research Institute (H.Z.), London, UK.
Raymund A RoosFrom the Huntington's Disease Research Centre (E.B.J., L.M.B., S.G., F.B.R., S.J.T., R.I.S., E.J.W.), UCL Institute of Neurology, London, UK; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institut du Cerveau et de la Moelle épinière (A.D.), Sorbonne Universités, UPMC University Paris 06, UMRS 1127, INSERM, U 1127, CNRS, UMR 7225; APHP (A.D.), Genetics Department, Pitié-Salpêtrière University Hospital, Paris, France; Centre for Molecular Medicine and Therapeutics (B.R.L.), University of British Columbia, Vancouver, BC, Canada; Department of Neurology (R.A.R.), Leiden University, the Netherlands; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; and UK Dementia Research Institute (H.Z.), London, UK.
Henrik ZetterbergFrom the Huntington's Disease Research Centre (E.B.J., L.M.B., S.G., F.B.R., S.J.T., R.I.S., E.J.W.), UCL Institute of Neurology, London, UK; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institut du Cerveau et de la Moelle épinière (A.D.), Sorbonne Universités, UPMC University Paris 06, UMRS 1127, INSERM, U 1127, CNRS, UMR 7225; APHP (A.D.), Genetics Department, Pitié-Salpêtrière University Hospital, Paris, France; Centre for Molecular Medicine and Therapeutics (B.R.L.), University of British Columbia, Vancouver, BC, Canada; Department of Neurology (R.A.R.), Leiden University, the Netherlands; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; and UK Dementia Research Institute (H.Z.), London, UK.
Sarah J TabriziFrom the Huntington's Disease Research Centre (E.B.J., L.M.B., S.G., F.B.R., S.J.T., R.I.S., E.J.W.), UCL Institute of Neurology, London, UK; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institut du Cerveau et de la Moelle épinière (A.D.), Sorbonne Universités, UPMC University Paris 06, UMRS 1127, INSERM, U 1127, CNRS, UMR 7225; APHP (A.D.), Genetics Department, Pitié-Salpêtrière University Hospital, Paris, France; Centre for Molecular Medicine and Therapeutics (B.R.L.), University of British Columbia, Vancouver, BC, Canada; Department of Neurology (R.A.R.), Leiden University, the Netherlands; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; and UK Dementia Research Institute (H.Z.), London, UK.
Rachael I ScahillFrom the Huntington's Disease Research Centre (E.B.J., L.M.B., S.G., F.B.R., S.J.T., R.I.S., E.J.W.), UCL Institute of Neurology, London, UK; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institut du Cerveau et de la Moelle épinière (A.D.), Sorbonne Universités, UPMC University Paris 06, UMRS 1127, INSERM, U 1127, CNRS, UMR 7225; APHP (A.D.), Genetics Department, Pitié-Salpêtrière University Hospital, Paris, France; Centre for Molecular Medicine and Therapeutics (B.R.L.), University of British Columbia, Vancouver, BC, Canada; Department of Neurology (R.A.R.), Leiden University, the Netherlands; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; and UK Dementia Research Institute (H.Z.), London, UK.
Edward J WildFrom the Huntington's Disease Research Centre (E.B.J., L.M.B., S.G., F.B.R., S.J.T., R.I.S., E.J.W.), UCL Institute of Neurology, London, UK; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institut du Cerveau et de la Moelle épinière (A.D.), Sorbonne Universités, UPMC University Paris 06, UMRS 1127, INSERM, U 1127, CNRS, UMR 7225; APHP (A.D.), Genetics Department, Pitié-Salpêtrière University Hospital, Paris, France; Centre for Molecular Medicine and Therapeutics (B.R.L.), University of British Columbia, Vancouver, BC, Canada; Department of Neurology (R.A.R.), Leiden University, the Netherlands; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; and UK Dementia Research Institute (H.Z.), London, UK. e.wild@ucl.ac.uk.
TRACK-HD Study Group
National Hospital for Neurology and Neurosurgery · GBLeiden University · NLUniversity College London · GBUniversity of British Columbia · CA
Funding
Medical Research Council MR/J003832/1Medical Research Council MR/K023268/1Medical Research Council MR/L012936/1Medical Research Council MR/M008592/1Medical Research Council MR/P007015/1Wellcome Trust
Abstract
objectiveNeurofilament light (NfL) protein in blood plasma has been proposed as a prognostic biomarker of neurodegeneration in a number of conditions, including Huntington disease (HD). This study investigates the regional distribution of NfL-associated neural pathology in HD gene expansion carriers.
methodsWe examined associations between NfL measured in plasma and regionally specific atrophy in cross-sectional (n = 198) and longitudinal (n = 177) data in HD gene expansion carriers from the international multisite TRACK-HD study. Using voxel-based morphometry, we measured associations between baseline NfL levels and both baseline gray matter and white matter volume; and longitudinal change in gray matter and white matter over the subsequent 3 years in HD gene expansion carriers.
resultsAfter controlling for demographics, associations between increased NfL levels and reduced brain volume were seen in cortical and subcortical gray matter and within the white matter. After also controlling for known predictors of disease progression (age and CAG repeat length), associations were limited to the caudate and putamen. Longitudinally, NfL predicted subsequent occipital gray matter atrophy and widespread white matter reduction, both before and after correction for other predictors of disease progression.
conclusionsThese findings highlight the value of NfL as a dynamic marker of brain atrophy and, more generally, provide further evidence of the strong association between plasma NfL level, a candidate blood biomarker, and pathologic neuronal change.
Indexed as
AdolescentAdultAtrophyBiomarkersBrainCross-Sectional StudiesDisease ProgressionDNA Repeat ExpansionFemaleFollow-Up StudiesGray MatterHeterozygoteHumansHuntingtin ProteinHuntington DiseaseLongitudinal StudiesBiomarkersHTT protein, humanHuntingtin Proteinneurofilament protein LNeurofilament Proteins
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