Behavioral deficits in APP(V717F) transgenic mice deficient for the apolipoprotein E gene.
Both the beta-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 Abeta rather than to amyloid deposits.
Dodart
J C
JC
Laboratoire d'Ethologie et Neurobiologie, Université Louis Pasteur, URA 1295 CNRS, Strasbourg, France.
Mathis
C
C
Bales
K R
KR
Paul
S M
SM
Ungerer
A
A
D000682:Amyloid / Q000378:metabolism; D016564:Amyloid beta-Protein Precursor / Q000235:genetics*; D000818:Animals; D001057:Apolipoproteins E / Q000172:deficiency* / Q000235:genetics; D001522:Behavior, Animal / Q000502:physiology*; D001921:Brain / Q000378:metabolism; D006801:Humans; D001523:Mental Disorders / Q000235:genetics*; D051379:Mice; D008815:Mice, Inbred Strains; D008822:Mice, Transgenic / Q000235:genetics; D009043:Motor Activity / Q000502:physiology; D009154:Mutation / Q000502:physiology*; D010364:Pattern Recognition, Visual / Q000502:physiology; D014018:Tissue Distribution
D000682:Amyloid; D016564:Amyloid beta-Protein Precursor; D001057:Apolipoproteins E