Tau levels in platelets isolated from Huntington's disease patients serve as a biomarker of disease severity.
Melanie Alpaugh, Juan Lantero-Rodriguez, Andrea L Benedet, Uriel Manseau, Martine Boutin, Massimo Maiuri, Helena L Denis, Maria Masnata, Shaline V Fazal, Sylvain Chouinard, Pedro Rosa-Neto, Roger A Barker, Kaj Blennow, Henrik Zetterberg, Richard Labib, Francesca Cicchetti
Author Information
Melanie Alpaugh: Department of Molecular and Cellular Biology, University of Guelph, Guelph, Canada. alpaughm@uoguelph.ca. ORCID
Juan Lantero-Rodriguez: Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
Andrea L Benedet: Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
Uriel Manseau: Department of Mathematical and Industrial Engineering, Polytechnique Montreal, Montreal, Canada.
Martine Boutin: Département de Psychiatrie & Neurosciences, Faculté de Médecine, Université Laval, Quebec, Canada.
Massimo Maiuri: Department of Molecular and Cellular Biology, University of Guelph, Guelph, Canada.
Helena L Denis: Département de Psychiatrie & Neurosciences, Faculté de Médecine, Université Laval, Quebec, Canada.
Maria Masnata: Département de Psychiatrie & Neurosciences, Faculté de Médecine, Université Laval, Quebec, Canada.
Shaline V Fazal: Department of Clinical Neurosciences, John Van Geest Centre for Brain Repair, University of Cambridge, Cambridge, UK.
Sylvain Chouinard: Department of Movement Disorders, Centre Hospitalier Universitaire de Montréal-Hôtel Dieu, CHUM, Montréal, Canada.
Pedro Rosa-Neto: Translational Neuroimaging Laboratory, McGill University Research Centre for Studies in Aging, Douglas Research Institute, Le Centre Intégré Universitaire de Santé et de Services Sociaux (CIUSSS) de l'Ouest-de-L'Île-de-Montréal, Montreal, Canada.
Roger A Barker: Department of Clinical Neurosciences, John Van Geest Centre for Brain Repair, University of Cambridge, Cambridge, UK.
Kaj Blennow: Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
Henrik Zetterberg: Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
Richard Labib: Department of Mathematical and Industrial Engineering, Polytechnique Montreal, Montreal, Canada.
Francesca Cicchetti: Département de Psychiatrie & Neurosciences, Faculté de Médecine, Université Laval, Quebec, Canada. francesca.cicchetti@crchudequebec.ulaval.ca.
Tau is a microtubule protein that is known to be hyperphosphorylated and to aggregate in several chronic neurodegenerative disorders. In many cases, in particular in Alzheimer's disease, the degree of tau pathology has been demonstrated to correlate with cognitive deficits and/or decline. In Huntington's disease (HD), a dominantly inherited neurodegenerative disorder, both cognitive impairments and abnormal tau expression have been reported to occur, along with the accumulation of the mutant huntingtin protein. In this respect, tau has been shown to be present in the cerebrospinal fluid of individuals with HD and to increase with disease progression. However, how this relates to changes in tau found in the periphery is largely unknown. In this study, we collected blood samples from patients with HD and isolated multiple blood components including plasma, platelets, and peripheral blood mononuclear cells to measure their tau levels and subsequently correlate these to cognitive impairments and disease stage. Our results suggest that the amount of tau, particularly N-terminal tau (NTA-tau) and total tau (t-tau), is elevated in all assayed blood components and that the quantity of tau within platelets, specifically, is strongly correlated with disease severity.
