Figure 1.

Proteomic analysis of SNCA-OVX midbrain demonstrates that mitochondrial dysfunction is a key factor in α-synuclein-induced neurodegeneration. a, Schematic representation of proteomics workflow. b, Pathway enrichment of dysregulated proteins in 18-month-old SNCA-OVX mice showing pathway enrichment (%) and enrichment significance (–log(p value)). c, Schematic representation on dysregulated mitochondrial complex I subunits caused by α-synuclein overexpression. Complex I subunits perturbed in SNCA-OVX mice (green) and subunits associated with mitochondrial diseases (red outline). d, Dysregulated proteins in SNCA-OVX mice, which are associated with altered α-synuclein levels. Upregulated/downregulated proteins are red/green, respectively, based on their magnitude of upregulation/downregulation. For dopaminergic cell and oligomeric analysis, see Extended Data Figure 1-1. For extended proteomic descriptors and validation, see Extended Data Figure 1-2.