The interaction of exosomal α-synuclein and microglial TLR2 has emerged as an important driving force for excessive microglial phagocytosis of α-synuclein, and exosomes derived from microglia have been suggested to be responsible for cell-to-cell transmission of pathological forms of α-synuclein, promoting the spread of PD [120]. This evidence concerns the gene SNCA and Parkinson disease.