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The main neuropathological hallmark of PD and DLB are inclusions, known as Lewy bodies (LBs), enriched not only in \u03b1-synuclein (aSyn), but also in lipid species, organelles, membranes, and even nucleic acids. Furthermore, several genetic risk factors for PD are mutations in genes involved in lipid metabolism, such as\n                    <jats:italic>GBA1<\/jats:italic>\n                    ,\n                    <jats:italic>VSP35<\/jats:italic>\n                    , or\n                    <jats:italic>PINK1<\/jats:italic>\n                    . Thus, it is not surprising that mechanisms that have been implicated in PD, such as inflammation, altered intracellular and vesicular trafficking, mitochondrial dysfunction, and alterations in the protein degradation systems, may be also directly or indirectly connected through lipid homeostasis. In this review, we highlight and discuss the recent evidence that suggests lipid biology as important drivers of PD, and which require renovated attention by neuropathologists. Particularly, we address the implication of lipids in aSyn accumulation and in the spreading of aSyn pathology, in mitochondrial dysfunction, and in ER stress. Together, this suggests we should broaden the view of PD not only as a proteinopathy but also as a lipidopathy.\n                  <\/jats:p>","DOI":"10.1007\/s00401-023-02601-0","type":"journal-article","created":{"date-parts":[[2023,7,8]],"date-time":"2023-07-08T06:01:56Z","timestamp":1688796116000},"page":"369-385","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":60,"title":["More than meets the eye in Parkinson\u2019s disease and other synucleinopathies: from proteinopathy to lipidopathy"],"prefix":"10.1007","volume":"146","author":[{"given":"Manuel","family":"Flores-Leon","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1679-1727","authenticated-orcid":false,"given":"Tiago Fleming","family":"Outeiro","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2023,7,8]]},"reference":[{"key":"2601_CR1","doi-asserted-by":"publisher","first-page":"239","DOI":"10.1016\/S0896-6273(00)80886-7","volume":"25","author":"A Abeliovich","year":"2000","unstructured":"Abeliovich A, Schmitz Y, Fari\u00f1as I, Choi-Lundberg D, Ho WH, Castillo PE et al (2000) Mice lacking alpha-synuclein display functional deficits in the nigrostriatal dopamine system. 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