Although these molecular and cellular changes are observed only in the kidney but not in the brain of LRRK2-/- mice, they bear striking resemblance to processes that are thought to be involved in PD pathogenesis, suggesting that LRRK2 mutations may cause Parkinson's disease and cell death via impairment of protein degradation pathways, leading to protein accumulation and aggregation over time. This evidence concerns the gene LRRK2 and Parkinson disease.