{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,2]],"date-time":"2026-06-02T20:22:42Z","timestamp":1780431762899,"version":"3.54.1"},"reference-count":0,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2013,1,1]],"date-time":"2013-01-01T00:00:00Z","timestamp":1356998400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Parkinson\u2019s Disease"],"published-print":{"date-parts":[[2013,8,1]]},"abstract":"<jats:p>Background: Multiple system atrophy (MSA) is a fatal neurodegenerative disease of unknown aetiology characterised by the accumulation of insoluble \u03b1-synuclein (\u03b1-syn) aggregates in the cytoplasm of myelin-producing oligodendrocytes. Dysfunction of the lipid-rich myelin membrane may precede \u03b1-syn pathology in MSA pathogenesis. ATP-binding cassette transporter A8 (ABCA8) is a little-studied lipid transporter, which has recently been found to be highly expressed in oligodendrocyte-rich white matter regions of the human brain. ABCA8 expression promotes sphingomyelin production in oligodendrocytes in vitro, suggesting a role in myelin formation and maintenance. Objective: We hypothesise that aberrant ABCA8 expression in oligodendrocytes plays a role in the early pathogenesis of MSA by impacting myelin stability and regulation of \u03b1-syn and p25\u03b1. Methods: We measured the expression of ABCA8, \u03b1-syn and p25\u03b1 in MSA brains in disease-affected grey matter (GM, putamen and cerebellum), disease-affected white matter (WM, under the motor cortex) and an unaffected brain region (visual cortex). We transfected human oligodendrocytes with ABCA8 and assessed its impact on \u03b1-syn and p25\u03b1 expression. Results: ABCA8 expression was significantly increased in the disease-affected GM and WM with no significant change in the unaffected brain region. \u03b1-syn and p25\u03b1 expression were significantly increased in the disease-affected WM and GM respectively. Overexpression of ABCA8 in oligodendrocytes caused significant increases in both \u03b1-syn and p25\u03b1 expression. Conclusions: These data suggest a direct relationship between the levels of ABCA8 and the ectopic expression of \u03b1-syn and increased expression of p25\u03b1. As these data reflect results found in MSA, we hypothesise that increased ABCA8 may precipitate MSA pathology.<\/jats:p>","DOI":"10.3233\/jpd-130203","type":"journal-article","created":{"date-parts":[[2019,12,3]],"date-time":"2019-12-03T13:58:19Z","timestamp":1575381499000},"page":"331-339","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":17,"title":["Increased Expression of ABCA8 in Multiple System Atrophy Brain is                     Associated with Changes in Pathogenic Proteins"],"prefix":"10.1177","volume":"3","author":[{"given":"Jonathan M.","family":"Bleasel","sequence":"first","affiliation":[{"name":"Neuroscience Research Australia, Sydney, NSW, Australia"},{"name":"School of Medical Sciences, University of New South Wales, Sydney, NSW,\r                    Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jen-Hsiang T.","family":"Hsiao","sequence":"additional","affiliation":[{"name":"Neuroscience Research Australia, Sydney, NSW, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Glenda M.","family":"Halliday","sequence":"additional","affiliation":[{"name":"Neuroscience Research Australia, Sydney, NSW, Australia"},{"name":"School of Medical Sciences, University of New South Wales, Sydney, NSW,\r                    Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Woojin Scott","family":"Kim","sequence":"additional","affiliation":[{"name":"Neuroscience Research Australia, Sydney, NSW, Australia"},{"name":"School of Medical Sciences, University of New South Wales, Sydney, NSW,\r                    Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2013,1,1]]},"container-title":["Journal of Parkinson\u2019s Disease"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.3233\/JPD-130203","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.3233\/JPD-130203","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T04:42:22Z","timestamp":1777610542000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.sagepub.com\/doi\/10.3233\/JPD-130203"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2013,1,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2013,8,1]]}},"alternative-id":["10.3233\/JPD-130203"],"URL":"https:\/\/doi.org\/10.3233\/jpd-130203","relation":{"is-cited-by":[{"id-type":"doi","id":"10.3389\/fnins.2019.01187","asserted-by":"object"},{"id-type":"doi","id":"10.1007\/978-3-319-67199-4_166","asserted-by":"object"},{"id-type":"doi","id":"10.1007\/s12035-015-9205-3","asserted-by":"object"},{"id-type":"doi","id":"10.1007\/978-1-4614-6438-9_166-1","asserted-by":"object"},{"id-type":"doi","id":"10.3389\/fnmol.2017.00356","asserted-by":"object"}]},"ISSN":["1877-7171","1877-718X"],"issn-type":[{"value":"1877-7171","type":"print"},{"value":"1877-718X","type":"electronic"}],"subject":[],"published":{"date-parts":[[2013,1,1]]}}}