Interestingly, validated mouse models for familial AD have shown disrupted spatial reference memory and object recognition [23]–[25] and deficiency in Abca1, which is one of the main ABC transporters and essential for cholesterol homeostasis, exacerbated amyloidogenesis in amyloid mouse models of AD [26], [27], whereas Abca1 overexpression ameliorated amyloid load [28]. This evidence concerns the gene ABCA1 and amyloidosis.