Importantly, activating PPARα not only upregulates the expression of Mfn2 and Plin5 but also promotes Mfn2-Plin5 tethering, re-establishing LD-mitochondrial coupling and facilitating LD catabolism in DA neurons, which ultimately rescues nigrostriatal DA neurodegeneration and alleviates motor deficits in CIH-exposed PD models. This evidence concerns the gene MFN2 and Parkinson disease.