Memories of intense, traumatic and unpleasant experiences are hard to forget. This persistence of so called ‘emotional memories’ is typically beneficial as it allows us to reflect on significant personal events and respond to future challenges effectively. However, if negative thoughts and experiences dominate our everyday lives, as is the case in major depression, then emotional memories can engulf our autobiographical histories, creating a chronic state of anxiety. Research suggests that sleep is crucial for emotional memory management. Restricted sleep impairs memory performance and psychological stability in healthy adults, while sleep disturbances are commonplace in major depression, affecting up to 90% of patients. A full understanding of the relationship between sleep, memory and emotion is therefore vital for gaining scientific insights into the mind, learning more about the fundamental biology of mental health and disease, and identifying innovative targets for therapeutic intervention. Combining behavioural testing, sleep polysomnography and fMRI, the aim of this project is to provide a systematic investigation of the mechanisms by which sleep processes emotional memories. This will offer new headway in disentangling the links between chronic sleep disturbances and emotional memory impairments in psychiatric conditions, and may lay the groundwork for innovative therapeutic interventions.
Obstructive Sleep Apnoea Syndrome (OSAS) affects 2-4% of men, 1-2% of women, and up to 15% of aging people (Gibson, 2005). It is characterised by repeated episodes of upper airway obstruction during sleep, resulting in hypoxia and disturbed sleep (Dempsey et al., 2010). OSAS is strongly linked to obesity (Arens et al., 2000), poor mental health (Grunstein et al., 1995) and impaired cognitive function (Nemeth et al., 2012; Engleman & Douglas, 2004), creating a substantial socio-economic burden. Sleep affects the consolidation process that strengthens newly formed memories (Rasch & Born, 2013). A strongly supported view is that newly encountered information is first stored temporarily in the hippocampus, with components of sleep such as “slow oscillations” (<1 Hz) promoting transfer to longer-term neocortical sites (Marshall & Born, 2007). However, few studies have examined memory consolidation in patients with OSAS (Cipelli et al., 2013) with even fewer incorporating measures of sleep EEG. In one exception, Guo et al. 2013) observed reduced overnight improvements in declarative memory that correlated with slow-wave sleep duration in 22 adults with OSAS, despite similar performance to controls prior to sleep. Overnight improvements in procedural memory tasks are also conspicuously absent, even when patients are matched with controls on alertness (Csabi, et al., 2014; Djonlagic et al., 2012; Kloepfer et al., 2009); however an absence of sleep EEG data in these studies means that group differences in procedural memory consolidation may not be sleep-dependent. OSAS is treated with Continuous Positive Airway Pressure (CPAP), requiring patients to wear a face mask during sleep to regulate breathing. Systematic reviews have confirmed moderate/large post-treatment improvements in sleepiness (Engleman & Douglas, 2004), and sleep efficiency/onset latency (Jenkinson et al.,1999; Ballester et al., 1999; Giles et al., 2006). Preliminary evidence also suggests that CPAP can lead to immediate changes in sleep architecture, including increased slow-wave sleep (Chikadze et al., 2013; McArdle & Douglas, 2001). However, we do not know if these benefits maintain over time and/or extend to memory consolidation. By addressing these gaps, the proposed research will have clear clinical value and broader benefits for advancing theories of sleep-dependent consolidation across patient and non-patient populations.
Recent research has provided good evidence that sleep has a role to play in consolidation of new declarative memories (for facts and words) in humans. However, we are still far from understanding how consolidation operates and why sleep is involved. One promising line of evidence has used external selective reactivation of memories during sleep. In this paradigm, participants first learn a set of new declarative memories (e.g., object-location mappings) and in the learning phase they hear sounds associated with each object (e.g., a miaow for a cat). During sleep, some of the new memories are reactivated by playing the same sounds embedded in noise, with the reactivated memories being better recalled after sleep. This external reactivation paradigm is a highly promising tool for studying memory consolidation. One possible explanation is that the external reactivation serves as a trigger for transferring new memories from temporary storage in the hippocampus to more permanent and robust storage in the neocortex of the brain. Alternatively, the reactivation may simply strengthen the existing representation without altering its location within the brain. Here we are exploring these possibilities in order to understand how memory consolidation works, how reactivation works, and in what circumstances sleep influences consolidation.