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This proteinopathy+lipidopathy paradigm has been further refined to a fatty acid (FA)\u2010opathy, centering dysregulated FA metabolism as fundamental in PD lipid dysfunction. FA dysfunction can disrupt alpha\u2010synuclein (\u03b1S)\u2010membrane interactions, altering \u03b1S localization, conformation, and aggregation. Correcting FA dyshomeostasis rescues PD\u2010associated \u03b1S phenotypes and is a promising strategy for disease\u2010modifying therapeutics. Herein, we consider the impact of PD FA dyshomeostasis in modifying the bioactive oxylipin\u2010ome. Oxylipin metabolism is complex, and the role of oxylipins in PD is not yet fully determined. This perspective considers PD\u2010associated differences oxylipin profiles, oxylipin precursor polyunsaturated fatty acids (PUFAs), and oxylipin biosynthetic enzymes in human PD studies to explore a potential PD oxylipin\u2010ome signature. Founded on disrupted oxylipin and oxylipin precursor PUFA abundance, higher PUFA intake reducing PD risk and progression, and the association between cyclooxygenase (COX) inhibition and lower PD incidence, we posit that the oxylipin\u2010ome plays a role in PD. Oxylipin metabolism may be a novel target for PD biomarkers and disease\u2010modifying therapeutics.<\/jats:p>","DOI":"10.1002\/advs.202522997","type":"journal-article","created":{"date-parts":[[2026,4,22]],"date-time":"2026-04-22T14:56:02Z","timestamp":1776869762000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["The Emerging Parkinson's Disease Oxylipin\u2010Ome"],"prefix":"10.1002","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5765-6129","authenticated-orcid":false,"given":"Julia C.","family":"Kelliher","sequence":"first","affiliation":[{"name":"Ann Romney Center for Neurologic Diseases Department of Neurology Brigham and Women's Hospital and Harvard Medical School  Boston Massachusetts 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