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

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Abstract
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.