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Recessive loss-of-function mutations in\n                    <jats:italic>ATP13A2<\/jats:italic>\n                    , a lysosomal transmembrane P5\n                    <jats:sub>B<\/jats:sub>\n                    -type ATPase and polyamine exporter, can cause early-onset familial PD. Familial\n                    <jats:italic>ATP13A2<\/jats:italic>\n                    mutations are also linked to related neurodegenerative diseases, including Kufor-Rakeb syndrome, hereditary spastic paraplegias, neuronal ceroid lipofuscinosis, and amyotrophic lateral sclerosis. Despite the severe effects of\n                    <jats:italic>ATP13A2<\/jats:italic>\n                    mutations in humans,\n                    <jats:italic>ATP13A2<\/jats:italic>\n                    knockout (KO) mice fail to exhibit neurodegeneration even at advanced ages, making it challenging to study the neuropathological effects of ATP13A2 loss in vivo. Germline deletion of\n                    <jats:italic>ATP13A2<\/jats:italic>\n                    in rodents may trigger the upregulation of compensatory pathways during embryonic development that mask the full neurotoxic effects of ATP13A2 loss in the brain. To explore this idea, we selectively deleted\n                    <jats:italic>ATP13A2<\/jats:italic>\n                    in the adult mouse brain by the unilateral delivery of an AAV-Cre vector into the substantia nigra of young adult mice carrying conditional\n                    <jats:italic>lox<\/jats:italic>\n                    P-flanked\n                    <jats:italic>ATP13A2<\/jats:italic>\n                    KO alleles. We observe a progressive loss of striatal dopaminergic nerve terminals at 3 and 10 months after AAV-Cre delivery. Cre-injected mice also exhibit robust dopaminergic neuronal degeneration in the substantia nigra at 10 months. Adult-onset\n                    <jats:italic>ATP13A2<\/jats:italic>\n                    KO also recreates many of the phenotypes observed in aged germline\n                    <jats:italic>ATP13A2<\/jats:italic>\n                    KO mice, including lysosomal abnormalities, p62-positive inclusions, and neuroinflammation. Our study demonstrates that the adult-onset homozygous deletion of\n                    <jats:italic>ATP13A2<\/jats:italic>\n                    in the nigrostriatal pathway produces robust and progressive dopaminergic neurodegeneration that serves as a useful in vivo model of\n                    <jats:italic>ATP13A2<\/jats:italic>\n                    -related neurodegenerative diseases.\n                  <\/jats:p>","DOI":"10.1038\/s41531-024-00748-5","type":"journal-article","created":{"date-parts":[[2024,7,19]],"date-time":"2024-07-19T20:03:44Z","timestamp":1721419424000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":20,"title":["Adult-onset deletion of ATP13A2 in mice induces progressive nigrostriatal pathway dopaminergic degeneration and lysosomal abnormalities"],"prefix":"10.1038","volume":"10","author":[{"given":"Madalynn L.","family":"Erb","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kayla","family":"Sipple","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nathan","family":"Levine","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xi","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2359-5679","authenticated-orcid":false,"given":"Darren J.","family":"Moore","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,7,20]]},"reference":[{"key":"748_CR1","doi-asserted-by":"publisher","first-page":"R48","DOI":"10.1093\/hmg\/ddp012","volume":"18","author":"S Lesage","year":"2009","unstructured":"Lesage, S. & Brice, A. 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