Both the beta-amyloid precursor protein (APP) and the apoliprotein E (apoE)
genes are involved in the pathogenesis of Alzheimer's disease (AD). We pre
viously showed that mice over-expressing a human mutated form of APP (APP(V
717F)) display age-dependent recognition memory deficits associated with th
e 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 am
yloid deposition, differ from APP(V717F) mice in the object recognition tas
k. The recognition performance is decreased in both transgenic mouse groups
compared to control groups.;Moreover, some behavioral disturbances display
ed 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 A beta rather than to amyloid deposit
s. NeuroReport 11:603-607 (C) 2000 Lippincott Williams & Wilkins.