Many daily functions require us to hold the information of events that happen for a sufficient period time (e.g. remember where the car is parked for a few hours). However, our ability of holding spatial memory declines with age. Cognitive ageing imposes negative impacts on the life quality in our later life. Facing a rapidly ageing population, such impacts extend from the individual to the families and the society as a whole. If we have a better understanding on how the memory decline occurs, we are in a stronger position to provide strategies to improve our memory retention, which will lead to a cognitively healthier society. To understand how daily memory decays naturally over time, we propose to model this in rodents. This is because they provide invaluable opportunities to understand the brain mechanisms, to control the environmental factors, and to draw unconfounded causative conclusions. Indeed, using this model we know that memory formation and maintenance occurs in multi-phases. As we encounter an event in a place we 'encode' the experience. It undergoes a biological process in the brain to 'consolidate' it so we remember it later. As we 'retrieve' that information some time later, the memory undergoes another process in the brain to 'reconsolidate' and we can remember it for longer. Importantly, we have identified a time window around the spatial memory encoding, during which we can introduce a novel event to make the memory last longer. This method of using novelty as a memory-facilitating event has so far only been proven to work in young animals. The first aim will determine whether the same strategy helps middle-aged and older animals. We will also explore more effective strategies to make memories last in older animals. It will also allow us to know whether the encoding and consolidation processes are differentially affected at different stages of ageing. In real life, we do not always have the chance to target the encoding and consolidation process as the event happens. It therefore would be beneficial if we can target the reconsolidation process during the time window of memory retrieval to make the memory last. Hence, the second aim of the study is to establish whether introducing a novel event around memory retrieval can subsequently make the memory last longer. We will examine whether this is an effective approach to make memory last in older animals. While the first 2 studies provide behavioural strategies to improve the longevity of memory at different ages, at present we do not know how the memory-encoding and memory-facilitating events interact at the cellular level in the brain. Previous research has pinpointed a key brain area, called the hippocampus that is crucial for linking events and place and form an episodic or associative memory. Previous theories also hypothesize that the cellular networks activated by the memory-encoding and memory-facilitating events are overlapping in the hippocampus that interactively contribute to longer-lasting memory. To visualise the cellular activities for these two events, we will mark the active cells with two fluorescence-labelled genes that can be detected by confocal microscopes. This technique has previously been established and will be carried out with our collaborator in Japan. Together, this project will allow us to establish behavioural methods to improve memory so that they last longer in old animals and characterise the underpinning encoding or consolidation process that is affected by ageing. We will also understand the cellular mechanism for the facilitation of memory persistence to occur. The behavioural strategy that we use in this project is non-invasive and benign, and therefore can be translated to human studies in the near future through cross-discipline collaborations. Such knowledge can ultimately improve cognitive ageing in the society.