Similarly, in an ‘environmental’ model of PD in wild-type rats, it was demonstrated that exposure to rotenone (which increased LRRK2 kinase activity as assessed by pThr73-Rab10 levels) could reproduce endolysosomal deficits seen in human post-mortem brains—and treatment with a LRRK2 kinase inhibitor could prevent them and thereby avert α-synuclein pathology and associated neurodegeneration115. This evidence concerns the gene LRRK2 and Parkinson disease.