Mice Homozygous for a Modified β‐Amyloid Precursor Protein (βAPP) Gene Show Impaired Behavior and High Incidence of Agenesis of the Corpus Callosuma

The amyloid precursor protein (βAPP) gene of the mouse was disrupted by homologous recombination; however, contrary to expectation, brain and other tissues still contained βAPP‐specific RNA, albeit at a level 5‐10 fold lower than wild‐type and lacking the disrupted exon, which had been spliced out. The brain contained shortened βAPP‐specific protein at a low level. Mutant mice were severely impaired in spatial learning and exploratory behavior and showed increased incidence of agenesis of the corpus callosum.