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Recently, loss-of-function mutations in the\n                    <jats:italic>ATP10B<\/jats:italic>\n                    gene have been identified in Parkinson\u2019s disease patients, pointing to\n                    <jats:italic>ATP10B<\/jats:italic>\n                    as a candidate genetic risk factor. Previous studies have shown compromised lysosomal functionality upon\n                    <jats:italic>ATP10B<\/jats:italic>\n                    knockdown in human cell lines and primary cortical neurons. To investigate the role of ATP10B in Parkinson\u2019s disease neuropathology, specifically in the nigrostriatal dopaminergic system, we induced ATP10B knockdown specifically in substantia nigra pars compacta neurons of rats using viral vector technology. Additionally, midbrain neuronal cultures derived from ATP10B knock-out human induced pluripotent stem cells clones were used to study the impact of ATP10B loss in dopaminergic neurons in a more translational model.\n                    <jats:italic>Atp10b<\/jats:italic>\n                    knockdown in rat brain induced parkinsonian motor deficits, and longitudinal striatal dopamine transporter\n                    <jats:sup>18<\/jats:sup>\n                    F-FE-PE2I PET imaging revealed a progressive decrease in binding potential. Immunohistochemical analysis conducted one year post-injection confirmed the loss of dopaminergic terminals in the striatum, alongside a loss of dopaminergic neurons in the substantia nigra pars compacta. The expression of LAMP1, LAMP2a, cathepsin B and glucocerebrosidase was studied in dopaminergic neurons. A decrease in lysosomal numbers and an increase in lysosomal volume were observed more consistently in one of the knockdown constructs. The vulnerability of dopaminergic neurons to ATP10B loss-of-function was also observed in midbrain neuronal cultures derived from ATP10B knock-out human induced pluripotent stem cells clones, which showed a significant reduction in TH-positive neurons. Taken together, our findings demonstrate that ATP10B depletion detrimentally impacts the viability of dopaminergic neurons both in vivo and in vitro. Moreover, a broader impact on the functionality of the nigrostriatal pathway was evidenced as rats with\n                    <jats:italic>Atp10b<\/jats:italic>\n                    knockdown exhibited motor impairments similar to those observed in Parkinson\u2019s disease patients.\n                  <\/jats:p>","DOI":"10.1007\/s00401-025-02908-0","type":"journal-article","created":{"date-parts":[[2025,7,17]],"date-time":"2025-07-17T17:46:01Z","timestamp":1752774361000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Loss of the lysosomal lipid flippase ATP10B leads to progressive dopaminergic neurodegeneration and parkinsonian motor deficits"],"prefix":"10.1007","volume":"150","author":[{"given":"Mar\u00eda","family":"Sanchiz-Calvo","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elena","family":"Coccia","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher","family":"Cawthorne","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gustavo","family":"Morrone Parfitt","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Teresa","family":"Torre-Muruzabal","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"George","family":"Tsafaras","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Koen","family":"Van Laere","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Diego","family":"Cabezudo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ana","family":"Cascalho","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chris","family":"Van den Haute","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Vangheluwe","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joel","family":"Blanchard","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eduard","family":"Bentea","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Veerle","family":"Baekelandt","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,7,17]]},"reference":[{"issue":"6","key":"2908_CR1","doi-asserted-by":"publisher","first-page":"523","DOI":"10.1016\/0024-3205(64)90161-4","volume":"3","author":"N-E And\u00e9n","year":"1964","unstructured":"And\u00e9n N-E, Carlsson A, Dahlstr\u00f6m A, Fuxe K, Hillarp N-\u00c5, Larsson K (1964) Demonstration and mapping out of nigro-neostriatal dopamine neurons. 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