This evidence is supported by postmortem brain tissue, cell culture and in vivo models of PD that show that exposure to PD toxins that affect mitochondrial function and expression of PD-associated mutants of DJ-1, PINK1, Parkin, LRRK2, and α-synuclein, induce converging mitochondrial pathology including impaired mitochondrial respiration, mitochondrial shape/structure, mitochondrial trafficking, regenerative capacity, biogenesis and turnover leading to chronic oxidative stress and activation of apoptotic pathways to promote neurodegeneration of SN neurons. The gene discussed is LRRK2; the disease is Parkinson disease.