Animal models of AD, such as Caenorhabditis elegans (CE) transgenic for human Aβ42 and TTR [77], and mice transgenic models for mutant forms of the amyloid β precursor protein (APP), expressing different levels of endogenous TTR or hTTR [78], have been widely used to dissect the mechanism behind the disease. This evidence concerns the gene TTR and Alzheimer disease.