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One of the proposed pathogenic mechanisms of \u03b1-syn mutations is mitochondrial dysfunction. However, it is not entirely clear the impact of impaired mitochondrial dynamics induced by \u03b1-syn on neurodegeneration and whether targeting this pathway has therapeutic potential. In this study we evaluated whether inhibition of mitochondrial fission is neuroprotective against \u03b1-syn overexpression\n                    <jats:italic>in vivo<\/jats:italic>\n                    . To accomplish this goal, we overexpressed human A53T-\u03b1- synuclein (hA53T-\u03b1-syn) in the rat nigrostriatal pathway, with or without treatment using the small molecule Mitochondrial Division Inhibitor-1 (mdivi-1), a putative inhibitor of the mitochondrial fission Dynamin-Related Protein-1 (Drp1). We show here that mdivi-1 reduced neurodegeneration, \u03b1-syn aggregates and normalized motor function. Mechanistically, mdivi-1 reduced mitochondrial fragmentation, mitochondrial dysfunction and oxidative stress. These\n                    <jats:italic>in vivo<\/jats:italic>\n                    results support the negative role of mutant \u03b1-syn in mitochondrial function and indicate that mdivi-1 has a high therapeutic potential for PD.\n                  <\/jats:p>","DOI":"10.1038\/s41598-017-07181-0","type":"journal-article","created":{"date-parts":[[2017,8,2]],"date-time":"2017-08-02T04:05:24Z","timestamp":1501646724000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":141,"title":["Mitochondrial division inhibitor-1 is neuroprotective in the A53T-\u03b1-synuclein rat model of Parkinson\u2019s disease"],"prefix":"10.1038","volume":"7","author":[{"given":"Simone","family":"Bido","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1229-9663","authenticated-orcid":false,"given":"Federico N.","family":"Soria","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rebecca Z.","family":"Fan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0410-4638","authenticated-orcid":false,"given":"Erwan","family":"Bezard","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6606-4371","authenticated-orcid":false,"given":"Kim","family":"Tieu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2017,8,8]]},"reference":[{"key":"7181_CR1","doi-asserted-by":"publisher","unstructured":"Rappold, P.M. et al. 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