Thereby, these findings suggest that TLR2 mediates astroglial α-synuclein accumulation through neuron-to-astroglial α-synuclein transmission and may contribute to local immune response in patients with DLB/PD, and that treatment with anti-TLR2 antibody might block the neuropathology by blocking NFκB and p38 MAPK signaling in astrocytes. This evidence concerns the gene NFKB1 and Parkinson disease.