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Early development of social deficits in APP and APP-PS1 mice.

Abstract：

: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.

journal_name

Neurobiol Aging

journal_title

Neurobiology of aging

authors

Pietropaolo S,Delage P,Lebreton F,Crusio WE,Cho YH

doi

10.1016/j.neurobiolaging.2011.09.012

subject

Has Abstract

pub_date

2012-05-01 00:00:00

pages

1002.e17-27

issue

5

eissn

0197-4580

issn

1558-1497

pii

S0197-4580(11)00349-6

journal_volume

33

pub_type

杂志文章

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