Abstract: Parkinson’s disease–A lipidopathy? The histopathological hallmark of Parkinson’s disease (PD) and dementia with Lewy bodies are inclusions enriched in α-synuclein (α-syn), known as Lewy bodies, which are not only composed of proteins, but also a core of lipid species. PD has been thus far principally thought of as a “proteinopathy” caused by the misfolding of α-syn. However, there is a major role for certain lipids in modulating α-syn physiology in the brain and both decreased and increased membrane interactions and interactions with specific fatty acids are potential triggers for α-syn oligomerization and fibril formation. Alterations in lipid homeostasis have been observed in several brain regions that show pathology and PD should be considered not only a proteinopathy but also a lipidopathy due to the following: 
1. Lipids/membranes are core components of Lewy bodies;
2. Lipid proportions in organelles affect the α-syn structure and lipid-binding properties; 
3. Lipid dyshomeostasis is linked to impaired organelle function;
4. Lipid accumulation in neurons and parenchyma are associated with neuroinflammation;
5. Lipid metabolism genes have been identified as risk factors for PD. 
Hence, a comprehensive analysis of the brain lipidome, in combination with genomics and proteomics, promises a more holistic view of brain chemistry and can aid in the discovery of biomarkers for diagnosing and monitoring diseases.