Finally, the idea that abnormalities in mitochondrial function are a critical step in initiating dopaminergic neuronal dysfunction, leading to parkinsonian phenotypes and, ultimately, to dementia associated with Lewy bodies (LBD), is also supported by the pathophysiological features displayed by genetic forms of PD, such as those associated with LRRK2, PRKN [86], and α-synuclein (SNCA) gene mutations, in which cognitive impairment is also described [109]. Here, PRKN is linked to Parkinson disease.