Spittau described these changes at the molecular level, including the TLR-dependent triggering of alpha-synuclein (αSyn), activation of microglia through neuromelanin, and αSyn deficient phagocytosis in PD, whereas in AD, the decrease in phagocytosis of the β-amyloid plaques (Aβ) and depletion of the microglia do not decrease the formation of plaques and neurodegeneration continues (Spittau, 2017). The gene discussed is SNCA; the disease is Parkinson disease.