In PD, this includes reported defects in the SNCA, PINK1 genes (associated with abnormal mitochondria and increased apoptosis), parkin (associated with impaired damaged protein tagging with ubiquitin), LRRK2 (associated with increased neuroinflammation) and DJ-1 (associated with increased reactive oxygen species), with genes such as APP (associated with the generation of beta-amyloid peptides), PSEN1 and PSEN2 (both interact with APP and are associated with the overproduction of toxic beta-amyloid peptides) displaying defects in AD [28,29,30,31]. This evidence concerns the gene APP and Alzheimer disease.