The present review summarizes converging evidence from animal and human studies that an early target of amyloid pathology is synaptic activity in the DG (dentate gyrus)/CA3 network. We briefly review the computational significance of the DG/CA3 network in the encoding of episodic memory and present new evidence that the CA3/DG pattern of activation is compromised in a mouse model of amyloid pathology. In addition, we present a new behavioural method to test the prediction that amyloid-related synaptic pathology will disrupt the formation of an integrated episodic-like (what, where and when) memory in mice.

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