Early hippocampal synaptic plasticity and episodic like-memory deficits in a transgenic mouse model of Alzheimer disease - involvment of corticosterone

Background The etiology of Alzheimer’s disease (AD) is unclear and no cure is yet available. The function of the hippocampus, a key structure responsible for memory encoding and consolidation, is affected early in AD leading to progressive irreversible memory loss. There is strong evidence that AD onset is, at least partly, due to accumulation within the hippocampus of peptides processed from the amyloid precursor protein APP, such as amyloid-beta (A?). Also, several studies demonstrated an abnormal elevation in the main stress hormone, cortisol (CORT in mice), in the initial phase of AD in patients and in mouse models. Here, we investigated if early co-accumulation of CORT and APP-derived peptides could be a main trigger driving the onset of memory deficits in AD.