Intraindividual Neurofilament Dynamics in Serum Mark the Conversion to Sporadic Parkinson's Disease.

Parkinson's disease (PD) biomarker longitudinal study neurofilament light chain (NfL) premanifest disease prodromal symptoms serum single molecule array (Simoa) technique

Journal

Movement disorders : official journal of the Movement Disorder Society
ISSN: 1531-8257
Titre abrégé: Mov Disord
Pays: United States
ID NLM: 8610688

Informations de publication

Date de publication:
07 2020
Historique:
received: 02 01 2020
revised: 23 02 2020
accepted: 03 03 2020
pubmed: 28 4 2020
medline: 28 4 2021
entrez: 28 4 2020
Statut: ppublish

Résumé

With disease-modifying treatment strategies on the horizon, stratification of individual patients at the earliest stages of Parkinson's disease (PD) is key-ideally already at clinical disease onset. Blood levels of neurofilament light chain (NfL) provide an easily accessible fluid biomarker that might allow capturing the conversion from prodromal to manifest PD. We assessed longitudinal serum NfL levels in subjects converting from prodromal to manifest sporadic PD (converters), at-risk subjects, and matched controls (72 participants with ≈4 visits), using single-molecule array (Simoa) technique. While NfL levels were not increased at the prodromal stage, subjects converting to the manifest motor stage showed a significant intraindividual acceleration of the age-dependent increase of NfL levels. The temporal dynamics of intraindividual NfL blood levels might mark the conversion to clinically manifest PD, providing a potential stratification biomarker for individual disease onset in the advent of precision medicine for PD. © 2020 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

Sections du résumé

BACKGROUND AND OBJECTIVES
With disease-modifying treatment strategies on the horizon, stratification of individual patients at the earliest stages of Parkinson's disease (PD) is key-ideally already at clinical disease onset. Blood levels of neurofilament light chain (NfL) provide an easily accessible fluid biomarker that might allow capturing the conversion from prodromal to manifest PD.
METHODS
We assessed longitudinal serum NfL levels in subjects converting from prodromal to manifest sporadic PD (converters), at-risk subjects, and matched controls (72 participants with ≈4 visits), using single-molecule array (Simoa) technique.
RESULTS
While NfL levels were not increased at the prodromal stage, subjects converting to the manifest motor stage showed a significant intraindividual acceleration of the age-dependent increase of NfL levels.
CONCLUSIONS
The temporal dynamics of intraindividual NfL blood levels might mark the conversion to clinically manifest PD, providing a potential stratification biomarker for individual disease onset in the advent of precision medicine for PD. © 2020 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

Identifiants

pubmed: 32338403
doi: 10.1002/mds.28026
doi:

Substances chimiques

Biomarkers 0
Neurofilament Proteins 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1233-1238

Commentaires et corrections

Type : CommentIn

Informations de copyright

© 2020 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

Références

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Auteurs

Carlo Wilke (C)

Department of Neurodegenerative Diseases, Hertie Institute for Clinical Brain Research and Center of Neurology, University of Tübingen, Tübingen, Germany.
German Center for Neurodegenerative Diseases, University of Tübingen, Tübingen, Germany.

Marcia Cristina Teixeira Dos Santos (MCT)

Experimental Medicine and Diagnostics, Global Exploratory Development, UCB Biopharma, Braine-L'Alleud, Belgium.

Claudia Schulte (C)

Department of Neurodegenerative Diseases, Hertie Institute for Clinical Brain Research and Center of Neurology, University of Tübingen, Tübingen, Germany.
German Center for Neurodegenerative Diseases, University of Tübingen, Tübingen, Germany.

Christian Deuschle (C)

Department of Neurodegenerative Diseases, Hertie Institute for Clinical Brain Research and Center of Neurology, University of Tübingen, Tübingen, Germany.
German Center for Neurodegenerative Diseases, University of Tübingen, Tübingen, Germany.

Dieter Scheller (D)

Consultancy Neuropharm, Neuss, Germany.

Moira Verbelen (M)

Exploratory Statistics, Global Exploratory Development, UCB Pharma, Slough, United Kingdom.

Kathrin Brockmann (K)

Department of Neurodegenerative Diseases, Hertie Institute for Clinical Brain Research and Center of Neurology, University of Tübingen, Tübingen, Germany.
German Center for Neurodegenerative Diseases, University of Tübingen, Tübingen, Germany.

Anna-Katharina von Thaler (AK)

Department of Neurodegenerative Diseases, Hertie Institute for Clinical Brain Research and Center of Neurology, University of Tübingen, Tübingen, Germany.
German Center for Neurodegenerative Diseases, University of Tübingen, Tübingen, Germany.

Ulrike Sünkel (U)

Department of Neurodegenerative Diseases, Hertie Institute for Clinical Brain Research and Center of Neurology, University of Tübingen, Tübingen, Germany.
German Center for Neurodegenerative Diseases, University of Tübingen, Tübingen, Germany.

Benjamin Roeben (B)

Department of Neurodegenerative Diseases, Hertie Institute for Clinical Brain Research and Center of Neurology, University of Tübingen, Tübingen, Germany.
German Center for Neurodegenerative Diseases, University of Tübingen, Tübingen, Germany.

Sarah Bujac (S)

Exploratory Statistics, Global Exploratory Development, UCB Pharma, Slough, United Kingdom.

Florian G Metzger (FG)

Department of Psychiatry and Psychotherapy, University Hospital Tübingen, Tübingen, Germany.
Geriatric Center, University Hospital Tübingen, Tübingen, Germany.
Vitos Hospital for Psychiatry and Psychotherapy, Haina, Germany.

Walter Maetzler (W)

Department of Neurodegenerative Diseases, Hertie Institute for Clinical Brain Research and Center of Neurology, University of Tübingen, Tübingen, Germany.
Department of Neurology, University Hospital Schleswig-Holstein, Kiel University, Kiel, Germany.

Andre Nogueira da Costa (AN)

Experimental Medicine and Diagnostics, Global Exploratory Development, UCB Biopharma, Braine-L'Alleud, Belgium.
Precision Medicine, Oncology R&D Organisation, AstraZeneca, Molndal, Sweden.

Matthis Synofzik (M)

Department of Neurodegenerative Diseases, Hertie Institute for Clinical Brain Research and Center of Neurology, University of Tübingen, Tübingen, Germany.
German Center for Neurodegenerative Diseases, University of Tübingen, Tübingen, Germany.

Daniela Berg (D)

Department of Neurodegenerative Diseases, Hertie Institute for Clinical Brain Research and Center of Neurology, University of Tübingen, Tübingen, Germany.
Department of Neurology, University Hospital Schleswig-Holstein, Kiel University, Kiel, Germany.

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