Large-scale proteomics profiling of peripheral blood of DM1 patients identifies biomarkers for disease severity and functional capacity
BackgroundMyotonic Dystrophy Type 1 (DM1), the most common genetic neuromuscular disorder in adults, poses significant challenges for drug development due to its multisystem nature and high clinical variability in symptoms and disease progression. With a growing number of therapies entering clinical trials, this study addresses the urgent need for biomarkers that can serve as surrogate endpoints.MethodsWe profiled 437 serum samples from adult DM1 patients collected at two timepoints of the OPTIMISTIC trial using bottom-up mass spectrometry with data-independent acquisition. Associations between protein expression, the disease-causing CTG-repeat and 25 clinical outcome measures were studied using linear mixed-effect models. All key study findings were validated in an independent cohort of 69 DM1 patients and 10 healthy controls.ResultsOf the 259 identified proteins, 161 showed significant associations with the CTG-repeat length (FDR < 5%). Hypogammaglobulinemia was confirmed and shown to be worse in severely affected patients. A strong proteomic signature was associated with clinical measures of functional capacity, with the 6-Minute Walk Test showing the strongest signal (70 associations, FDR < 5%). These novel associations reveal a compelling link between chronic inflammation and reduced functional capacity. A machine learning algorithm identified a minimal set of 13 proteins robustly reflecting both the underlying genetic defect and functional capacity.ConclusionsDM1 induces a broad disease fingerprint in the serum proteome, predominantly affecting proteins of the immune system. A carefully selected panel of proteins showed the greatest potential to meet the statistical criteria required for surrogate endpoints in clinical trials.
Authors
- Alain J. van Gool (ORCID: https://orcid.org/0000-0003-0010-5286)
- Daniël van As (ORCID: https://orcid.org/0000-0002-4702-1330)
- Renee Salz (ORCID: https://orcid.org/0000-0003-1035-7866)
- Lennart Martens (ORCID: https://orcid.org/0000-0003-4277-658X)
- Delphi Van Haver (ORCID: https://orcid.org/0000-0002-4659-5631)
- Geneviève Gourdon (ORCID: https://orcid.org/0000-0002-3319-1347)
- Tine Claeys (ORCID: https://orcid.org/0000-0001-9408-488X)
- Baziel G.M. van Engelen (ORCID: https://orcid.org/0000-0001-9867-9047)
- Sara Dufour
- Élise Duchesne (ORCID: https://orcid.org/0000-0002-9953-8315)
- Vera Dobelmann
- Ralf Gabriels
- Francis Impens
- Amber van Deelen
- Tobias Ruck
- Benedikt Schoser
- Andrea Gangfuss
- Hanns Lochmüller
- Jolein Gloerich
- Pieter Jan Volders
- Andreas Roos
- Cynthia Gagnon
- Guillaume Bassez
Institutions
- Centre National de la Recherche Scientifique (FR)
- Université de Sherbrooke (CA)
- Radboud University Nijmegen (NL)
- University of Ottawa (CA)
- Ottawa Hospital (CA)
- Ghent University Hospital (BE)
- University Medical Center (US)
- Radboud University Medical Center (NL)
- Sorbonne Université (FR)
- Düsseldorf University Hospital (DE)
- Centre Intégré Universitaire de Santé et de Services Sociaux du Saguenay–Lac-Saint-Jean (CA)
- Jessa Hospital (BE)
- Assistance Publique – Hôpitaux de Paris (FR)
- University Clinic of Traumatology (AT)
- Pitié-Salpêtrière Hospital (FR)
- Centre for Interdisciplinary Research in Rehabilitation (CA)
- Qatar Cardiovascular Research Center (QA)
- BG University Hospital Bergmannsheil Bochum (DE)
- VIB-UGent Center for Medical Biotechnology (BE)
- Université Laval (CA)
- Centre de Recherche en Myologie
- Heinrich Heine University Düsseldorf (DE)
- University of Duisburg-Essen (DE)
- Université de Strasbourg (FR)
Publication Details
- Journal
- Journal of Neuromuscular Diseases
- Published
- 2026-01-16
- DOI
- https://doi.org/10.1177/22143602251410443
- Primary Topic
- Genetic Neurodegenerative Diseases
- Type
- article
- Field-Weighted Citation Impact
- 0.00