Early development of social deficits in APP and APP-PS1 mice
Neurobiology of Aging. 2012-05-01; 33(5): 1002.e17-1002.e27
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Pietropaolo S(1), Delage P, Lebreton F, Crusio WE, Cho YH.
(1)University Bordeaux, INCIA, UMR 5287, F-33400 Talence, France.
Mimicking relevant behavioral features of the human pathology is one of the most
important challenges for animal models of neurological disorders including
Alzheimer disease (AD). Indeed, the most popular genetic AD mouse lines bearing
mutations of the amyloid precursor protein (APP) and presenilin 1 genes (PS1),
often fail to present robust cognitive deficits or show them only at very
advanced ages. It is therefore crucial to identify AD-like behavioral alterations
which may reliably reflect the early stages of the pathology, thus permitting
tests of more efficient early therapeutic interventions. Here, we demonstrated
the very early expression of noncognitive AD-like symptoms, i.e., deficits in
social interest, interaction and communication, in APP and APP-PS1 transgenic
mice. Conversely, other noncognitive behaviors (sensori-motor gating) as well as
cognitive abilities (spontaneous alternation) were unaltered in AD transgenics.
Our data suggest that social deficits precede other neuropsychiatric and
cognitive AD-like symptoms and can be employed as early markers of AD pathology
in genetic mouse models.