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To date, there is no disease-modifying therapy available for these synucleinopathies. Furthermore, the intracellular mechanisms by which \u03b1Syn confers toxicity are not yet fully understood. Therefore, it is of utmost importance to investigate the pathophysiology of \u03b1Syn-induced toxicity in order to identify novel molecular targets for the development of disease-modifying therapies.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We performed the first genome-wide siRNA modifier screening in a human postmitotic neuronal cell model using \u03b1Syn-induced toxicity as a read-out. In a multi-step approach, we identified several genes, whose knockdown protected against \u03b1Syn-induced toxicity. The main hit was further validated by different methods, including immunofluorescence microscopy, qPCR, and Western blot. Furthermore, the main finding was confirmed in mouse primary neurons.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The highest protection was achieved by knockdown of\n                      <jats:italic>SNX5<\/jats:italic>\n                      , which encodes the sorting nexin 5 (SNX5) protein, a component of the retromer complex. The protective efficacy of\n                      <jats:italic>SNX5<\/jats:italic>\n                      knockdown was confirmed with an independent siRNA system. The protective effect of\n                      <jats:italic>SNX5<\/jats:italic>\n                      knockdown was further confirmed in primary neurons from transgenic mice, where the knockdown of\n                      <jats:italic>SNX5<\/jats:italic>\n                      led to amelioration of decrease in synchrony that was observed in untreated and control-siRNA-treated cells. SNX5 protein is a component of the SNX-BAR (Bin\/Amphiphysin\/Rvs) heterodimer, which is part of the retromer complex. Extracellular \u03b1Syn and overexpression of intracellular \u03b1Syn led to fragmentation of the trans-Golgi network, which was prevented by\n                      <jats:italic>SNX5<\/jats:italic>\n                      knockdown that led to confinement of \u03b1Syn in early endosomes.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>In summary, our data suggest that SNX5 plays an important role in the trafficking and toxicity of \u03b1Syn. Therefore, SNX5 appears to be a target of therapeutic intervention for synucleinopathies.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s40035-025-00486-5","type":"journal-article","created":{"date-parts":[[2025,6,2]],"date-time":"2025-06-02T23:02:11Z","timestamp":1748905331000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["A genome-wide RNA interference screening reveals protectiveness of SNX5 knockdown in a Parkinson\u2019s disease cell model"],"prefix":"10.1186","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5333-0121","authenticated-orcid":false,"given":"Matthias","family":"H\u00f6llerhage","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linghan","family":"Duan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oscar Wing Ho","family":"Chua","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claudia","family":"Moebius","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Svenja H.","family":"Bothe","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kristina","family":"Losse","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rebecca","family":"Kotzur","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kristina","family":"Lau","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Franziska","family":"Hopfner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Franziska","family":"Richter","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christian","family":"Wahl-Schott","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marc","family":"Bickle","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G\u00fcnter U.","family":"H\u00f6glinger","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,6,3]]},"reference":[{"issue":"1","key":"486_CR1","doi-asserted-by":"publisher","first-page":"13","DOI":"10.1038\/nrneurol.2012.242","volume":"9","author":"M Goedert","year":"2013","unstructured":"Goedert M, Spillantini MG, Del Tredici K, Braak H. 100 years of Lewy pathology. 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