During learning, patterns of neuronal activity translate information about the external world into a sequence of internal representations. The representations are stored and subsequently processed across different areas of the brain. In the healthy brain recall cues can reactivate these representations, retrieving a specific memory event.
As memory processes are compromised in dementia and related disabilities the question arises as to whether dysfunctional internal representations in specific dementia-like disorders can be identified, thereby opening opportunities to target them with new therapies? A widely held view is that changes at the level of the synapse are key in the genesis of these representations.
While it is reasoned that temporal and spatial regulation of synaptic weight provides a scalar quantity to control information storage and retrieval, how this is affected in real-time in vivo for dementia-like disorders has not been investigated. In collaboration with Professor Bito at the University of Tokyo and Professor Sasaguri, RIKEN, the Emptage group will explore how synaptic engrams are formed and modified in knock-in Alzheimer disease (AD) mouse models with human familial AD mutations.