Our research focused on whether LRRK2 R1628P mutation altered the LRRK2 kinase activity, and caused subsequent neuronal death directly, or the pathogenic mechanisms of R1628P in PD involve a genotype-environment interaction, that R1628P genetic mutation of LRRK2 provided a potential two-hit target of environment toxic-induced Cdk5 activation. This evidence concerns the gene LRRK2 and Parkinson disease.