Marthe Gurine Førland1, Annika Öhrfelt2, Ingvild Dalen3, Ole-Bjørn Tysnes4, Kaj Blennow5, Henrik Zetterberg6, Kenn Freddy Pedersen7, Guido Alves8, Johannes Lange9. 1. The Norwegian Centre for Movement Disorders, Stavanger University Hospital, PO Box 8100, 4068, Stavanger, Norway. 2. Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Sahlgrenska University Hospital at Mölndal, University of Gothenburg, 43180, Mölndal, Sweden. 3. Section of Biostatistics, Department of Research, Stavanger University Hospital, PO Box 8100, 4068, Stavanger, Norway. 4. Department of Neurology, Haukeland University Hospital, PO Box 1400, 5021, Bergen, Norway; Institute for Clinical Medicine, University of Bergen, PO Box 1400, 5021, Bergen, Norway. 5. Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Sahlgrenska University Hospital at Mölndal, University of Gothenburg, 43180, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, 43180, Mölndal, Sweden. 6. Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Sahlgrenska University Hospital at Mölndal, University of Gothenburg, 43180, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, 43180, Mölndal, Sweden; Department of Molecular Neuroscience, UCL Institute of Neurology, University College London, Gower Street, WC1E 6BT, London, UK; UK Dementia Research Institute, Box 16, National Hospital for Neurology and Neurosurgery, Queen Square, WC1N 3BG, London, UK. 7. The Norwegian Centre for Movement Disorders, Stavanger University Hospital, PO Box 8100, 4068, Stavanger, Norway; Department of Neurology, Stavanger University Hospital, PO Box 8100, 4068, Stavanger, Norway. 8. The Norwegian Centre for Movement Disorders, Stavanger University Hospital, PO Box 8100, 4068, Stavanger, Norway; Department of Neurology, Stavanger University Hospital, PO Box 8100, 4068, Stavanger, Norway; Department of Mathematics and Natural Sciences, University of Stavanger, Stavanger, Norway. 9. The Norwegian Centre for Movement Disorders, Stavanger University Hospital, PO Box 8100, 4068, Stavanger, Norway. Electronic address: johannes.lange@sus.no.
Abstract
INTRODUCTION: Cerebrospinal fluid (CSF) total α-synuclein is considered a potential biomarker for Parkinson's disease (PD), but little is known about the evolution of this marker during the course of the disease. Our objective was to investigate whether CSF total α-synuclein concentrations change over time and are associated with motor and cognitive function in PD. METHODS: CSF total α-synuclein concentrations were quantified in 56 longitudinally followed PD patients, 27 of whom provided CSF repeatedly 2 and/or 4 years later. Another 18 subjects were included as controls. The samples were analyzed using two independent, validated ELISA methods: our recently developed and validated in-house ELISA and a commercial kit from BioLegend. RESULTS: CSF total α-synuclein levels did not distinguish PD patients from controls, displayed no substantial changes during a period of up to 4 years, and did not predict subsequent motor or cognitive decline. These findings were consistent for both analytical methods. CONCLUSION: Our findings do not support the clinical utility of total α-synuclein as a single diagnostic or prognostic biomarker in PD.
INTRODUCTION: Cerebrospinal fluid (CSF) total α-synuclein is considered a potential biomarker for Parkinson's disease (PD), but little is known about the evolution of this marker during the course of the disease. Our objective was to investigate whether CSF total α-synuclein concentrations change over time and are associated with motor and cognitive function in PD. METHODS: CSF total α-synuclein concentrations were quantified in 56 longitudinally followed PDpatients, 27 of whom provided CSF repeatedly 2 and/or 4 years later. Another 18 subjects were included as controls. The samples were analyzed using two independent, validated ELISA methods: our recently developed and validated in-house ELISA and a commercial kit from BioLegend. RESULTS: CSF total α-synuclein levels did not distinguish PDpatients from controls, displayed no substantial changes during a period of up to 4 years, and did not predict subsequent motor or cognitive decline. These findings were consistent for both analytical methods. CONCLUSION: Our findings do not support the clinical utility of total α-synuclein as a single diagnostic or prognostic biomarker in PD.
Authors: Mahsa Dolatshahi; Shayan Pourmirbabaei; Aida Kamalian; Amir Ashraf-Ganjouei; Mehdi Yaseri; Mohammad H Aarabi Journal: Front Neurol Date: 2018-07-11 Impact factor: 4.003
Authors: Brit Mollenhauer; Chelsea J Caspell-Garcia; Christopher S Coffey; Peggy Taylor; Andy Singleton; Leslie M Shaw; John Q Trojanowski; Mark Frasier; Tanya Simuni; Alex Iranzo; Wolfgang Oertel; Andrew Siderowf; Daniel Weintraub; John Seibyl; Arthur W Toga; Caroline M Tanner; Karl Kieburtz; Lana M Chahine; Kenneth Marek; Douglas Galasko Journal: Mov Disord Date: 2019-07-30 Impact factor: 10.338