Interestingly, significantly decreased levels of Par3, which interacts with Willin/FRMD6, are found in AD patients and are associated with impairments in APP trafficking that lead to intracellular accumulation of Aβ [145], potentially through a mechanism involving aPKC and dysregulated BACE1 trafficking in endosomes [144]. This evidence concerns the gene FRMD6 and Alzheimer disease.