Introduction: Neurodegenerative disorders such as Alzheimer’s disease (AD) are increasingly prevalent amongst older populations. Sleep irregularities are one of the chief complaints in people diagnosed with sleep disorders. Sleep has been hypothesized to ensure metabolic homeostasis and remove neurotoxic waste. Inadequate sleep leads to an accumulation of Amyloid-Beta (Aβ) levels which is associated with neurodegenerative diseases including AD and other dementias. Sleep is the driver of the glymphatic system, located in the perivascular space. The glymphatic system eliminates soluble proteins, including Aβ, from the central nervous system; transporting cerebrospinal fluid through the brain; and distributing macromolecules across the brain. This research proposal aims to identify optimal sleep patterns that decrease neurodegeneration by increasing glymphatic system functioning. Methods: This study will be an ad-hoc study conducted over a 6-month period utilizing participants who have reported a family history of AD. Aß accumulation and cortisol levels will be measured to identify signs of neurodegeneration using brain scans, such as Positron Emission Tomography, and blood tests. Other parameters such as memory, energy rating, and sleep latency will be measured. Results: Reduced slow-wave sleep may lead to a disruption in the glymphatic system. Monophasic sleep is said to have the most slow-wave sleep, and least rapid eye movement sleep which is most similar to wakefulness. Therefore, we hypothesize that monophasic sleep will slow neurodegeneration compared to biphasic and polyphasic sleep, contrary to popular belief that biphasic sleep is more beneficial than monophasic sleep. Discussion: In this experiment, we expect to see increased glymphatic clearance after monophasic sleep. There are many factors that can impact sleep patterns and glymphatic clearance including work style, environment, culture, race, sex, and genetic markers for AD. Conclusion: Further research that applies this suggested methodology should account for these variabilities when making conclusions on the optimal sleep pattern for plaque clearance in the brain. This proposal may improve research on AD by identifying the effects different sleep patterns have on the brain and neurodegeneration. Future research may study changes in sleep habits as a preventative measure for individuals who are at risk for or have been diagnosed with AD.
Introduction Stress is a known contributor to immune system suppression associated with higher illness susceptibility, including acute infectious respiratory illness, or the common cold. Sleep quality, shown to impact immunity, is an additional mechanism that may underlie the association between stress and cold symptomatology. Although the associations between stress and sleep and cold symptomatology have been examined separately, little is known about the mechanistic role of sleep in these associations. The present study examined sleep quality as a potential pathway between stress and cold symptomatology difference scores. Methods Archival data from the Common Cold Project (Pittsburgh Cold Study 3) were utilized for the present study. Participants were 213 adults (Mean Age=30.1 yrs., SD=10.9 yrs., 42.3% female) who completed a 5-day viral challenge and self-report measures of cold severity (Jackson Symptom Score; measured from beginning to end of viral challenge), baseline sleep quality (PSQI), and perceived stress as part of study participation. SPSS v 27 and Hayes’ PROCESS mediation macro were used to assess study aims. Age and sex were included as covariates. Results Greater perceived stress was significantly associated with worse sleep quality [B=.15, 95% CI .10, .21]. Sleep quality fully mediated the association between stress and changes in symptomatology; better sleep was associated with larger changes in cold severity [B=-.23, 95% CI -.43, -.04], defined as differences in symptomatology from beginning to end of the viral challenge, beyond stress alone. Zero-order correlation analyses revealed a trend level (r=.04, p=.06) association between sleep quality and aggregate cold severity, suggesting that as sleep improves, symptoms decrease. Conclusion Within the present sample, sleep quality surfaced as an indirect pathway linking stress to changes in cold severity. Better sleep was associated with greater changes in cold severity above perceived stress. These findings, together with the trend level, positive association between sleep quality and cold symptomatology, suggest that better sleep may be associated with less severe symptomatology. Future research should attend to mechanisms underlying the associations between stress, sleep, and cold symptomatology. Support (if any):
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