LRRK2 and Parkinson disease: Several aspects of mitochondrial dysfunction, such as increased oxidative stress, reduced mitochondria membrane potential, abnormal mitochondrial fission and fusion, and defects in mitochondrial trafficking, have been suggested from postmortem analysis of LRRK2-linked PD patient tissues [91] and from induced pluripotent stem cells (iPSCs)-derived neural cells from PD patients with LRRK2 mutation [92].