{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T04:56:57Z","timestamp":1790312217601,"version":"4.1.0"},"reference-count":38,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2017,5,29]],"date-time":"2017-05-29T00:00:00Z","timestamp":1496016000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001665","name":"Agence Nationale de la Recherche","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001665","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Movement Disorders"],"published-print":{"date-parts":[[2017,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    <jats:bold>Background<\/jats:bold>\n                    : MSA is a fatal neurodegenerative disorder characterized by a combination of autonomic dysfunction, cerebellar ataxia, and\n                    <jats:sc>l<\/jats:sc>\n                    \u2010dopa unresponsive parkinsonism. The hallmark of MSA is the accumulation of \u03b1\u2010synuclein, forming cytoplasmic inclusions in oligodendrocytes. Adeno\u2010associated viruses allow efficient targeting of disease\u2010associated genes in selected cellular ensembles and have proven efficient for the neuronal overexpression of \u03b1\u2010synuclein in the substantia nigra in the context of PD.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Objectives<\/jats:bold>\n                    : We aimed to develop viral\u2010based models of MSA.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Methods<\/jats:bold>\n                    : Chimeric viral vectors expressing either human wild\u2010type \u03b1\u2010synuclein or green fluorescent protein under the control of mouse myelin basic protein were injected in the striatum of rats and monkeys. Rats underwent a longitudinal motor assessment before histopathological analysis at 3 and 6 months.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Results<\/jats:bold>\n                    : Injection of vectors expressing \u03b1\u2010synuclein in the striatum resulted in &gt;80% oligodendroglial selectivity in rats and &gt;60% in monkeys. Rats developed progressive motor deficits that were\n                    <jats:sc>l<\/jats:sc>\n                    \u2010dopa unresponsive when assessed at 6 months. Significant loss of dopaminergic neurons occurred at 3 months, further progressing at 6 months, together with a loss of striatal neurons. Prominent \u03b1\u2010synuclein accumulation, including phosphorylated and proteinase\u2010K\u2013resistant \u03b1\u2010synuclein, was detected in the striatum and substantia nigra.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusions<\/jats:bold>\n                    : Viral\u2010mediated oligodendroglial expression of \u03b1\u2010synuclein allows replicating some of the key features of MSA. This flexible strategy can be used to investigate, in several species, how \u03b1\u2010synuclein accumulation in selected oligodendroglial populations contributes to the pathophysiology of MSA and offers a new framework for preclinical validation of therapeutic strategies. \u00a9 2017 International Parkinson and Movement Disorder Society\n                  <\/jats:p>","DOI":"10.1002\/mds.27041","type":"journal-article","created":{"date-parts":[[2017,5,29]],"date-time":"2017-05-29T06:16:46Z","timestamp":1496038606000},"page":"1230-1239","source":"Crossref","is-referenced-by-count":50,"title":["Viral\u2010mediated oligodendroglial alpha\u2010synuclein expression models multiple system atrophy"],"prefix":"10.1002","volume":"32","author":[{"given":"Fares","family":"Bassil","sequence":"first","affiliation":[{"name":"Universit\u00e9 de Bordeaux, Institut des Maladies Neurod\u00e9g\u00e9n\u00e9ratives, UMR 5293 Bordeaux France"},{"name":"CNRS, Institut des Maladies Neurod\u00e9g\u00e9n\u00e9ratives, UMR 5293 Bordeaux France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul A.","family":"Guerin","sequence":"additional","affiliation":[{"name":"Universit\u00e9 de Bordeaux, Institut des Maladies Neurod\u00e9g\u00e9n\u00e9ratives, UMR 5293 Bordeaux France"},{"name":"CNRS, Institut des Maladies Neurod\u00e9g\u00e9n\u00e9ratives, UMR 5293 Bordeaux France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nathalie","family":"Dutheil","sequence":"additional","affiliation":[{"name":"Universit\u00e9 de Bordeaux, Institut des Maladies Neurod\u00e9g\u00e9n\u00e9ratives, UMR 5293 Bordeaux France"},{"name":"CNRS, Institut des Maladies Neurod\u00e9g\u00e9n\u00e9ratives, UMR 5293 Bordeaux France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qin","family":"Li","sequence":"additional","affiliation":[{"name":"China Academy of Medical Sciences, Institute of Lab Animal Sciences Beijing China"},{"name":"Motac neuroscience Ltd Manchester United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthias","family":"Klugmann","sequence":"additional","affiliation":[{"name":"Translational Neuroscience Facility and Department of Physiology, School of Medical Sciences, UNSW Australia Sydney NSW Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2172-7527","authenticated-orcid":false,"given":"Wassilios G.","family":"Meissner","sequence":"additional","affiliation":[{"name":"Universit\u00e9 de Bordeaux, Institut des Maladies Neurod\u00e9g\u00e9n\u00e9ratives, UMR 5293 Bordeaux France"},{"name":"CNRS, Institut des Maladies Neurod\u00e9g\u00e9n\u00e9ratives, UMR 5293 Bordeaux France"},{"name":"Service de Neurologie, CHU de Bordeaux Bordeaux France"},{"name":"Centre de r\u00e9f\u00e9rence atrophie multisyst\u00e9matis\u00e9e, CHU de Bordeaux Bordeaux France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erwan","family":"Bezard","sequence":"additional","affiliation":[{"name":"Universit\u00e9 de Bordeaux, Institut des Maladies Neurod\u00e9g\u00e9n\u00e9ratives, UMR 5293 Bordeaux France"},{"name":"CNRS, Institut des Maladies Neurod\u00e9g\u00e9n\u00e9ratives, UMR 5293 Bordeaux France"},{"name":"China Academy of Medical Sciences, Institute of Lab Animal Sciences Beijing China"},{"name":"Motac neuroscience Ltd Manchester United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pierre\u2010Olivier","family":"Fernagut","sequence":"additional","affiliation":[{"name":"Universit\u00e9 de Bordeaux, Institut des Maladies Neurod\u00e9g\u00e9n\u00e9ratives, UMR 5293 Bordeaux France"},{"name":"CNRS, Institut des Maladies Neurod\u00e9g\u00e9n\u00e9ratives, UMR 5293 Bordeaux 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