In in vivo study of transgenic murine model of α-synucleinopathies (ASP), mice overexpressed human α-synuclein (hAS) with TLR4 deficiency (AS/TLR4−/−) exhibited severer neuronal loss, motor disability, and predominant reduced phagocytic activity than those with normal TLR4 expression(AS/TLR4+/+). The gene discussed is TLR4; the disease is synucleinopathy.