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Recent work has identified impairments in oligodendrocyte maturation as a novel and robust feature of SCA3 pathogenesis. Oligodendrocytes synthesize myelin structural components through the endoplasmic reticulum (ER), rendering this organelle essential for white matter integrity. Despite this, the role of ER function in SCA3 remains unclear. In this study, we show that loss of FICD-mediated AMPylation, a post-translational modification regulating the ER-resident HSP70 chaperone, BiP, rescues motor impairments in a transgenic SCA3 mouse model.\n                  <jats:italic>Ficd<\/jats:italic>\n                  <jats:sup>-\/-<\/jats:sup>\n                  SCA3 mice exhibit significantly reduced levels of nuclear ATXN3 in vulnerable brain regions, while\n                  <jats:italic>Ficd<\/jats:italic>\n                  <jats:sup>+\/+<\/jats:sup>\n                  littermates show an increased burden of AMPylated BiP in the spinal cord, identifying aberrant AMPylation as a novel contributor of SCA3 pathology. Using unbiased proteomics, we demonstrate that\n                  <jats:italic>Ficd<\/jats:italic>\n                  deletion mitigates the pathological decrease in myelin structural proteins and oligodendrocyte maturation factors, restoring levels of mature, myelinating oligodendrocytes. In parallel, we show that\n                  <jats:italic>Ficd<\/jats:italic>\n                  activates SREBP2-dependent cholesterol biosynthesis to support myelination. Taken as a whole, these findings posit ER homeostasis as a critical driver of oligodendrocyte pathology and identify FICD as a novel target for alleviating non-neuronal toxicity in SCA3.\n                <\/jats:p>","DOI":"10.64898\/2026.08.07.743629","type":"posted-content","created":{"date-parts":[[2026,8,10]],"date-time":"2026-08-10T15:05:21Z","timestamp":1786374321000},"source":"Crossref","is-referenced-by-count":0,"title":["<i>Ficd<\/i>\n                  loss rescues motor impairments and reverses oligodendrocyte maturation deficits in a mouse model of spinocerebellar ataxia type 3"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6892-9658","authenticated-orcid":false,"given":"Kate M.","family":"Van Pelt","sequence":"first","affiliation":[{"name":"Program in Cellular and Molecular Biology, University of Michigan, Ann Arbor, MI, 48109, USA"},{"name":"Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, 48109, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yamei","family":"Deng","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Michigan, Ann Arbor, MI, 48109, USA"},{"name":"Department of Computational Medicine & Bioinformatics, University of Michigan, Ann Arbor, MI, 48109, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2806-7819","authenticated-orcid":false,"given":"Alexey I.","family":"Nesvizhskii","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Michigan, Ann Arbor, MI, 48109, USA"},{"name":"Department of Computational Medicine & Bioinformatics, University of Michigan, Ann Arbor, MI, 48109, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0382-7535","authenticated-orcid":false,"given":"Henry L.","family":"Paulson","sequence":"additional","affiliation":[{"name":"Department of Neurology, 109 Zina Pitcher Place, University of Michigan, Ann Arbor, MI, 48109, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8466-4864","authenticated-orcid":false,"given":"Maria do Carmo","family":"Costa","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, College of Human Medicine, Michigan State University, East Lansing, MI, 48824, USA"},{"name":"Formerly: Department of Neurology, 109 Zina Pitcher Place, University of Michigan, Ann Arbor, MI, 48109, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0536-7923","authenticated-orcid":false,"given":"Matthias C.","family":"Truttmann","sequence":"additional","affiliation":[{"name":"Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, 48109, USA"},{"name":"Geriatrics Center, University of Michigan, Ann Arbor, MI, 48109, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"54368","reference":[{"key":"2026081120351570000_2026.08.07.743629v1.1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-pathmechdis-012418-012857"},{"key":"2026081120351570000_2026.08.07.743629v1.2","doi-asserted-by":"publisher","DOI":"10.1016\/j.nbd.2019.104635"},{"key":"2026081120351570000_2026.08.07.743629v1.3","doi-asserted-by":"publisher","DOI":"10.1038\/nrn.2017.92"},{"key":"2026081120351570000_2026.08.07.743629v1.4","doi-asserted-by":"publisher","DOI":"10.1016\/B978-0-444-51892-7.00027-9"},{"key":"2026081120351570000_2026.08.07.743629v1.5","doi-asserted-by":"publisher","DOI":"10.1007\/s12311-011-0340-8"},{"key":"2026081120351570000_2026.08.07.743629v1.6","doi-asserted-by":"publisher","DOI":"10.1097\/WCO.0b013e3282f7673d"},{"key":"2026081120351570000_2026.08.07.743629v1.7","doi-asserted-by":"crossref","first-page":"202","DOI":"10.1002\/acn3.156","article-title":"Survival and severity in dominant cerebellar ataxias","volume":"2","year":"2015","journal-title":"Ann Clin Transl Neurol"},{"key":"2026081120351570000_2026.08.07.743629v1.8","doi-asserted-by":"publisher","DOI":"10.1111\/jnc.14541"},{"key":"2026081120351570000_2026.08.07.743629v1.9","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.biochem.78.082307.091526"},{"key":"2026081120351570000_2026.08.07.743629v1.10","doi-asserted-by":"publisher","DOI":"10.1016\/j.molcel.2011.05.036"},{"key":"2026081120351570000_2026.08.07.743629v1.11","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(00)80943-5"},{"key":"2026081120351570000_2026.08.07.743629v1.12","doi-asserted-by":"crossref","unstructured":"L. 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