{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T14:26:55Z","timestamp":1785421615417,"version":"3.56.0"},"posted":{"date-parts":[[2026,6,16]]},"group-title":"Neuroscience","reference-count":82,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,6,16]],"date-time":"2026-06-16T00:00:00Z","timestamp":1781568000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.biorxiv.org\/about\/FAQ#license"}],"funder":[{"award":["R01NS086778"],"award-info":[{"award-number":["R01NS086778"]}],"id":[{"id":"https:\/\/ror.org\/01cwqze88","id-type":"ROR","asserted-by":"publisher"}]},{"name":"Sastry Foundation Endowed Chair in Parkinson Disease Research","award":["-"],"award-info":[{"award-number":["-"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,6,16]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:sec>\n                  <jats:title>Background<\/jats:title>\n                  <jats:p>While \u03b1-synuclein (\u03b1-syn) accumulation and iron dysregulation are hallmarks of Parkinson\u2019s Disease, the adaptations that enable neuronal survival under chronic protein stress remain unclear. Here, we investigated how \u03b1-syn overexpression and ceruloplasmin (Cp)-mediated iron modulation alters iron and redox homeostasis.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>We utilized human BE(2)-M17 neuroblastoma cell lines stably expressing different levels of \u03b1-syn to examine the interplay between \u03b1-syn, Ceruloplasmin (Cp)-mediated iron modulation, and the cellular response to oxidative stress. Analyses included Western blotting, immunofluorescence staining, soluble\/insoluble fractionation, glutathione, reactive oxygen species (ROS) and hydrogen peroxide (H\u2082O\u2082) quantification, lipid peroxidation, ferrous iron, and cell viability.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>Our data suggest an unexpected relationship between chronic \u03b1-syn expression and cellular redox regulation. Despite carrying a greater \u03b1-syn burden, cells with higher \u03b1-syn expression exhibit lower basal ROS, H\u2082O\u2082, and lipid peroxidation compared to control cells. These changes are not accompanied by activation of canonical antioxidant pathways suggesting that the reduced oxidative profile arises through alternative mechanisms. Besides, \u03b1-syn over-expressing cells display significant remodeling of iron-handling pathways, including altered expression of ferritin heavy chain, transferrin receptor, and ferroportin, suggesting that chronically high \u03b1-syn levels are associated with changes in iron homeostasis. In addition, this phenotype is not maintained following Cp overexpression. Although Cp reduces Fe\u00b2\u207a levels, it also induces substantial increases in ROS and H\u2082O\u2082 without corresponding changes in GPX4, glutathione, or related antioxidant systems. Thus, the reduced basal oxidative profile observed in \u03b1-syn-over-expressing cells does not reflect enhanced canonical antioxidant capacity. Instead, chronically high \u03b1-syn levels appear to be associated with adaptive remodeling of iron and redox pathways that become sensitive to oxidative imbalance.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>Chronic \u03b1-syn over-expression promotes adaptive remodeling of iron and redox homeostasis, associated with reduced basal oxidative stress but increased sensitivity to Cp-mediated perturbation. These data link \u03b1-syn burden to iron metabolism and stress-dependent vulnerability in synucleinopathies.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Graphical abstract<\/jats:title>\n                  <jats:fig id=\"ufig1\" position=\"float\" orientation=\"portrait\" fig-type=\"figure\">\n                    <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"732494v1_ufig1\" position=\"float\" orientation=\"portrait\"\/>\n                  <\/jats:fig>\n                <\/jats:sec>","DOI":"10.64898\/2026.06.15.732494","type":"posted-content","created":{"date-parts":[[2026,6,16]],"date-time":"2026-06-16T21:20:17Z","timestamp":1781644817000},"source":"Crossref","is-referenced-by-count":0,"title":["Chronic \u03b1-Synuclein Over-Expression and Ceruloplasmin Challenge Promote Distinct Iron and Redox Responses in M17 Cells"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9804-2046","authenticated-orcid":false,"given":"Masoumeh","family":"Pourhadi","sequence":"first","affiliation":[{"name":"Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bedri","family":"Ranxhi","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seth P.","family":"Sukuria","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fatimah H.","family":"Hussein","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201, USA"},{"name":"Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4399-5549","authenticated-orcid":false,"given":"Sokol V.","family":"Todi","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201, USA"},{"name":"Department of Neurology, Wayne State University School of Medicine, Detroit, MI 48201, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter A.","family":"LeWitt","sequence":"additional","affiliation":[{"name":"Department of Neurology, Wayne State University School of Medicine, Detroit, MI 48201, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9136-2581","authenticated-orcid":false,"given":"Wei-Ling","family":"Tsou","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"54368","reference":[{"issue":"9996","key":"2026061808051192000_2026.06.15.732494v1.1","doi-asserted-by":"crossref","first-page":"896","DOI":"10.1016\/S0140-6736(14)61393-3","article-title":"Parkinson\u2019s disease","volume":"386","year":"2015","journal-title":"The lancet"},{"key":"2026061808051192000_2026.06.15.732494v1.2","doi-asserted-by":"publisher","DOI":"10.1038\/s41593-019-0457-5"},{"issue":"1","key":"2026061808051192000_2026.06.15.732494v1.3","doi-asserted-by":"crossref","first-page":"29","DOI":"10.1186\/s13024-019-0329-1","article-title":"Alpha-synuclein structure and Parkinson\u2019s disease\u2013lessons and emerging principles","volume":"14","year":"2019","journal-title":"Molecular neurodegeneration"},{"key":"2026061808051192000_2026.06.15.732494v1.4","doi-asserted-by":"publisher","DOI":"10.1111\/jnc.13580"},{"key":"2026061808051192000_2026.06.15.732494v1.5","doi-asserted-by":"crossref","unstructured":"Mahoney-Sanchez L , Bouchaoui H , Boussaad I , Jonneaux A , Timmerman K , Berdeaux O , et al. 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