It has been hypothesized that the onset and progression of PD, unclear thus far, is dependent on the conjugation of different key factors such as neuroinflammation, alpha-synuclein induced neuronal dysfunction (through intracellular aggregation into Lewy bodies, which stand as the pathological hallmark of PD), systemic chronic inflammation (translated in the dysregulation of circulating inflammatory cytokines) and even gut and periodontal dysbiosis6,7. This evidence concerns the gene SNCA and Parkinson disease.