Future studies may integrate different pharmacological and lifestyle interventions aiming at positively modulating chronic inflammation and pathological alpha-synuclein aggregation as tightly interwoven processes in the pathogenesis of Parkinson’s disease and may focus on specific patient strata that can be defined genetically (e.g. LRRK2) or based on environmental factors (e.g. dysbiosis) and are enriched for the underlying chronic inflammatory process. This evidence concerns the gene SNCA and Parkinson disease.