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ABSTRACT: Objective
Deficits in social recognition and learning of social cues are major symptoms of neurodegenerative disorders such as Alzheimer's disease (AD). Here we studied the role of β1-noradrenergic signaling in cognitive function to determine whether it could be used as a potential therapeutic target for AD.Methods
Using pharmacological, biochemical and behavioral tools, we assessed social recognition and the β1-adrenergic receptor (ADR) and its downstream PKA/phospho-CREB (pCREB) signaling cascade in the medial amygdala (MeA) in Thy1-hAPPLond/Swe+(APP) mouse model of AD.Results
Our results demonstrated that APP mice display a significant social recognition deficit which is dependent on the β1-adrenergic system. Moreover,
SUBMITTER: Coutellier L
PROVIDER: S-EPMC4036739 | biostudies-literature | 2014 May
REPOSITORIES: biostudies-literature