Behavioral deficits in APPV717F transgenic mice decient for the apolipoprotein E gene

Abstract

Both the β-amyloid precursor protein (APP) and the apoliprotein E (apoE) genes are involved in the pathogenesis of Alzheimer's disease (AD). We previously showed that mice over-expressing a human mutated form of APP (APP^V717F) display age-dependent recognition memory deficits associated with the progression of amyloid deposition. Here, we asked whether 10-to 12-month-old APP^V717F mice lacking the apoE gene, which do not present obvious amyloid deposition, differ from APP^V717F mice in the object recognition task. The recognition performance is decreased in both transgenic mouse groups compared to control groups. Moreover, some behavioral disturbances displayed by APP mice lacking apoE are even more pronounced than those of APP mice expressing apoE. Our results suggest that the recognition memory deficits are related to high levels of soluble Aβ rather than to amyloid deposits.