The interconnectedness of the proposed pathomechanisms of PD (α-synuclein aggregation, endosome-related pathologies, and mitochondrial impairment) to neuroinflammation has been demonstrated for α-synuclein pathology (Li et al. 2019), increased LRRK2 activity (Lee et al. 2017), GCase alterations (Sanyal et al. 2020), and PRKN/PINK1-related mitochondrial dysfunction (Borsche et al. 2020). This evidence concerns the gene LRRK2 and Parkinson disease.