Triple-Knockout, Synuclein-Free Mice Display Compromised Lipid Pattern

Recent studies have implicated synucleins in several reactions during the biosynthesis of lipids and fatty acids addition to their recognised role membrane lipid binding synaptic functions. These are among aspects decreased synuclein functions that still poorly acknowledged especially regard pathogenesis Parkinson’s disease. Here, we aimed add existing knowledge deficiency (i.e., lack all three family members), with respect changes plasma, liver, two brain regions triple synuclein-knockout (TKO) mice. We describe long-chain polyunsaturated (LCPUFA) palmitic acid liver reduced triacylglycerol (TAG) accumulation non-esterified plasma free In midbrain, observed counterbalanced relative concentrations phosphatidylcholine (PC) cerebrosides (CER). also recorded a notable reduction ethanolamine plasmalogens midbrain mice, which is an important finding since abnormal ether metabolism usually associated neurological disorders. summary, our data demonstrates results alterations PUFA synthesis, storage CER, those polar principal compounds rafts many tissues. An ablation members causes more profound than previously shown be γ-synuclein alone. Possible mechanisms by may govern reported modifications TKO mice proposed discussed.