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Stage-dependent biomarker changes in spinocerebellar ataxia type 3.
Faber, Jennifer; Berger, Moritz; Carlo, Wilke; Hübener-Schmid, Jeannette; Schaprian, Tamara; Santana, Magda M; Grobe-Einsler, Marcus; Onder, Dement; Koyak, Berkan; Giunti, Paola; Garcia-Moreno, Hector; Gonzalez-Robles, Cristina; Lima, Manuela; Raposo, Mafalda; Melo, Ana Rosa Vieira; de Almeida, Luis Pereira; Silva, Patrick; Pinto, Maria M; van de Warrenburg, Bart P; van Gaalen, Judith; de Vries, Jeroen; Oz, Gulin; Joers, James M; Synofzik, Matthis; Schöls, Ludger; Riess, Olaf; Infante, Jon; Manrique, Leire; Timmann, Dagmar; Thieme, Andreas; Jacobi, Heike; Reetz, Kathrin; Dogan, Imis; Onyike, Chiadikaobi; Povazan, Michal; Schmahmann, Jeremy; Ratai, Eva-Maria; Schmid, Matthias; Klockgether, Thomas.
Afiliação
  • Faber J; German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
  • Berger M; Department of Neurology, University Hospital Bonn, Bonn, Germany.
  • Carlo W; University of Bonn, Medical Faculty, Institute for Medical Biometry, Informatics and Epidemiology.
  • Hübener-Schmid J; Division Translational Genomics of Neurodegenerative Diseases, Hertie Institute for Clinical Brain Research & Center of Neurology, University of Tübingen, Germany.
  • Schaprian T; German Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany.
  • Santana MM; Institute for Medical Genetics and Applied Genomics, University of Tuebingen, Tuebingen, Germany.
  • Grobe-Einsler M; German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
  • Onder D; Center for Neuroscience and Cell Biology (CNC), University of Coimbra, Coimbra, Portugal.
  • Koyak B; Center for Innovative in Biomedicine and Biotechnology (CIBB), University of Coimbra, Coimbra, Portugal.
  • Giunti P; German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
  • Garcia-Moreno H; Department of Neurology, University Hospital Bonn, Bonn, Germany.
  • Gonzalez-Robles C; German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
  • Lima M; Department of Neurology, University Hospital Bonn, Bonn, Germany.
  • Raposo M; German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
  • Melo ARV; Department of Neurology, University Hospital Bonn, Bonn, Germany.
  • de Almeida LP; Ataxia Centre, Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.
  • Silva P; Department of Neurogenetics, National Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, London WC1N 3BG, UK.
  • Pinto MM; Ataxia Centre, Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.
  • van de Warrenburg BP; Department of Neurogenetics, National Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, London WC1N 3BG, UK.
  • van Gaalen J; Ataxia Centre, Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.
  • de Vries J; Department of Neurogenetics, National Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, London WC1N 3BG, UK.
  • Jeroen; Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.
  • Oz G; Faculdade de Ciências e Tecnologia, Universidade dos Açores, Ponta Delgada, Portugal.
  • Joers JM; Faculdade de Ciências e Tecnologia, Universidade dos Açores, Ponta Delgada, Portugal.
  • Synofzik M; Instituto de Biologia Molecular e Celular (IBMC), Instituto de Investigação e Inovação em Saúde (i3S), Universidade do Porto, Porto, Portugal.
  • Schöls L; Faculdade de Ciências e Tecnologia, Universidade dos Açores, Ponta Delgada, Portugal.
  • Riess O; Center for Neuroscience and Cell Biology (CNC), University of Coimbra, Coimbra, Portugal.
  • Infante J; Center for Innovative in Biomedicine and Biotechnology (CIBB), University of Coimbra, Coimbra, Portugal.
  • Manrique L; Center for Neuroscience and Cell Biology (CNC), University of Coimbra, Coimbra, Portugal.
  • Timmann D; Center for Innovative in Biomedicine and Biotechnology (CIBB), University of Coimbra, Coimbra, Portugal.
  • Thieme A; Faculty of Pharmacy, University of Coimbra, Azinhaga de Santa Comba, 3000-548 Coimbra, Portugal.
  • Jacobi H; Center for Neuroscience and Cell Biology (CNC), University of Coimbra, Coimbra, Portugal.
  • Reetz K; Center for Innovative in Biomedicine and Biotechnology (CIBB), University of Coimbra, Coimbra, Portugal.
  • Dogan I; Faculty of Pharmacy, University of Coimbra, Azinhaga de Santa Comba, 3000-548 Coimbra, Portugal.
  • Onyike C; Department of Neurology, Donders Institute for Brain, Cognition, and Behaviour, Radboud university medical center.
  • Povazan M; Department of Neurology, Donders Institute for Brain, Cognition, and Behaviour, Radboud university medical center.
  • Schmahmann J; Department of Neurology, Rinjstate Hospital, Arnhem, The Netherlands.
  • Ratai EM; German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
  • Schmid M; Department of Neurology, University Hospital Bonn, Bonn, Germany.
  • Klockgether T; University of Bonn, Medical Faculty, Institute for Medical Biometry, Informatics and Epidemiology.
medRxiv ; 2023 Apr 25.
Article em En | MEDLINE | ID: mdl-37163081
Spinocerebellar ataxia type 3/Machado-Joseph disease (SCA3) is the most common autosomal dominant ataxia. In view of the development of targeted therapies for SCA3, precise knowledge of stage-dependent fluid and MRI biomarker changes is needed. We analyzed cross-sectional data of 292 SCA3 mutation carriers including 57 pre-ataxic individuals, and 108 healthy controls from the European Spinocerebellar ataxia type 3/Machado-Joseph Disease Initiative (ESMI) cohort. Blood concentrations of mutant ATXN3 and neurofilament light (NfL) were determined, and volumes of pons, cerebellar white matter (CWM) and cerebellar grey matter (CGM) were measured on MRI. Mutant ATXN3 concentrations were high before and after ataxia onset, while NfL continuously increased and deviated from normal 11.9 years before onset. Pons and CWM volumes decreased, but the deviation from normal was only 2.0 years (pons) and 0.3 years (CWM) before ataxia onset. We propose a staging model of SCA3 that includes an initial asymptomatic carrier stage followed by the biomarker stage defined by absence of ataxia, but a significant rise of NfL. The biomarker stage leads into the ataxia stage, defined by manifest ataxia. The present analysis provides a robust framework for further studies aiming at elaboration and differentiation of the staging model of SCA3.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: MedRxiv Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: MedRxiv Ano de publicação: 2023 Tipo de documento: Article