In particular, extensively studied transgenic AD models, such as mice overexpressing β-amyloid precursor protein (APP, disputably but generally accepted contributing factor to AD), PS1 and PS2 (expressing mutated presenilin-1 and presenilin-2, respectively), APP/PS1 (harboring human transgenes for both APP and PS1 together) and Tg2676 (overexpressing a mutant form of APP), do not demonstrate the expected loss of neural cells (Duff et al., 1996; Oyama et al., 1998; Elder et al., 2010). This evidence concerns the gene PSEN1 and Alzheimer disease.