We suggest here that sustained neuroinflammation promoting the spread of amyloidogenic S100A9 in the brain tissues can be a trigger of the amyloid cascade involving α-syn and leading to PD development [11], similar to the effect of S100A9 on Aβ aggregation in the Alzheimer’s disease [18]. The gene discussed is S100A9; the disease is early-onset autosomal dominant Alzheimer disease.