MYD88 and Parkinson disease: In summary, our novel observations suggest that overexpression of human mutated A53T α-synuclein in the vagus nerve could induce abnormal deposition of p-α-synuclein in SCs, initiating local neuroinflammation through activating the TLR2/MyD88/NF-κB signaling pathway, eliciting ultrastructural lesions in SCs and replicating the AutD characteristics of prodromal PD.