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Although multiple system atrophy (MSA), a devastating and rapidly progressing atypical parkinsonian disorder, is distributed equally among sexes, sex\u2010specific differences have been reported regarding autonomic dysfunctions, severity of motor symptoms, and survival rate, suggesting a need for sex\u2010specific treatment approaches. Neuroinflammation is a prominent hallmark in MSA pathology. Distinct activation patterns and increased phagocytosis of central nervous system (CNS) myeloid cells were observed, indicating a damaging role in this disease. In our previous study, we showed that colony\u2010stimulating factor 1 receptor (CSF1R)\u2013mediated depletion of myeloid cells in a mouse model of MSA led to a two\u2010faced outcome, comprised of a prolonged survival and delayed onset of neurological dystonia\u2010like symptoms, but also an aggravated motor phenotype and loss of dopaminergic neurons. Here, we re\u2010analyzed our previous findings to study sex\u2010specific effects in MSA in the presence and absence of CNS myeloid cells. Intriguingly, myeloid cell depletion was initially more effective in male animals. Although no sex\u2010specific effects were detected in motor behavior, the occurrence of dystonia\u2010like neurological symptoms was reduced, and neuronal loss was alleviated in male animals. Together, our findings provide insight into sex\u2010specific differences of CSF1R\u2010mediated myeloid cell depletion in MSA, emphasizing the need to study sex\u2010specific treatment strategies in neurodegenerative disorders.<\/jats:p>","DOI":"10.1111\/ejn.70586","type":"journal-article","created":{"date-parts":[[2026,6,19]],"date-time":"2026-06-19T03:17:54Z","timestamp":1781839074000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Sex\u2010Dependent Effects of CSF1R\u2010Mediated Myeloid Cell Depletion in a Mouse Model of Multiple System Atrophy"],"prefix":"10.1111","volume":"63","author":[{"given":"Kristina","family":"Battis","sequence":"first","affiliation":[{"name":"Department of Molecular Neurology University Hospital Erlangen, Friedrich\u2010Alexander\u2010Universit\u00e4t Erlangen\u2010N\u00fcrnberg  Erlangen 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Medicine of the University of Southern California  San Diego California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Xiang","sequence":"additional","affiliation":[{"name":"Department of Molecular Neurology University Hospital Erlangen, Friedrich\u2010Alexander\u2010Universit\u00e4t Erlangen\u2010N\u00fcrnberg  Erlangen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert A.","family":"Rissman","sequence":"additional","affiliation":[{"name":"Department of Physiology and Neuroscience Keck School of Medicine of the University of Southern California  San Diego California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0630-9204","authenticated-orcid":false,"given":"J\u00fcrgen","family":"Winkler","sequence":"additional","affiliation":[{"name":"Department of Molecular Neurology University Hospital Erlangen, Friedrich\u2010Alexander\u2010Universit\u00e4t 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