Early Treatment of Circadian Dysfunction for the Prevention of Alzheimer’s Disease
By: Angelica Schroeder
While we all know how important sleep is for our physical and mental health being that whether chronic or acute, we have all experienced the detrimental effects of sleep deprivation at some point in our lives, some might be surprised to learn that the neurological effects of a prolonged disruption of sleep and consequently a disruption of circadian rhythms have been implicated in the development of the neurodegenerative disease known as Alzheimer’s Disease. Previously, the sleep disturbances observed as a symptom of Alzheimer’s were seen as just that, as a symptom of the disease rather than a causal or predictive antecedent, however, recent studies have established substantial evidence for the pathological role of the prolonged disruption of the circadian sleep cycle (Musiek, Xiong, & Holtzman, 2015). Examining the presence of sleep disturbances among individuals with Alzheimer’s through this novel lens might ultimately provide greater insight into the underlying causes of this disease, and may subsequently lead to discovering preventative measures for this disease.
A primary reason why the sleep-wake cycle is of such importance with regard to the pathology of Alzheimer’s Disease is that a quite evident physical symptom exists with regard to the development of Alzheimer’s Disease being the presence of beta amyloid plaques. Beta amyloid is a metabolic byproduct, or metabolic waste, in the brain which is largely eliminated through the lymphatic system during sleep; we see that individuals with Alzheimer’s somewhere along the line begin to experience a disruption in this elimination of beta amyloid as evidenced by a buildup of this metabolic byproduct in the form of plaques which ultimately damage neurons potentially contributing to the severe cognitive deficits observed in patients with Alzheimer’s. A recent study examining this buildup of beta amyloid plaques found a correlation between the quality of sleep and beta amyloid deposits; in this study, researchers measured beta amyloid levels in the interstitial fluid of mice before inducing sleep deprivation (Musiek et al., 2015). Researchers in this study ultimately found that mice produced more beta amyloid during wakefulness and less beta amyloid while asleep, and that induction of sleep deprivation delayed the normal decrease in beta amyloid production which occurs near the usual onset of sleep (Musiek et al., 2015). This study was subsequently emulated in human subjects by measuring the beta amyloid levels in subject’s cerebrospinal fluid throughout the sleep-wake cycle, these findings were also consistent with the correlation between quality of sleep and beta amyloid deposits demonstrated in the previous study using mice. These findings are quite indicative of the importance of adequate sleep in allowing the body remove these metabolic wastes accumulated throughout the period of wakefulness, without proper removal we see an excess of these metabolic wastes which may ultimately lead to decreased efficiency with regard to brain function.
Now that we have discussed how irregular sleep patterns can disrupt circadian processes which may in turn contribute to the development of Alzheimer’s, I will now discuss irregular sleep patterns and deprivation as a consequence of Alzheimer’s Disease. Individuals with Alzheimer’s demonstrate a disturbance in sleep-wake patterns characterized by decreased sleep at night and increased sleep during the day; these irregular sleeping patterns ultimately lead the individual to engage in less sleep overall; this schedule also decreases the amount of our highly important slow wave sleep, as well as rapid eye movement sleep (Musiek et al., 2015). Rapid eye movement sleep has been shown to play an important role in learning and memory, which is the primary cognitive area severely affected by this disease. During slow wave sleep there is a decrease in the production of beta amyloid due to decreased neuronal firing in a period of neuronal hyperpolarization, therefore, a decrease in slow wave sleep ultimately leads to an increased production of beta amyloid. While this sporadic pattern of sleep would prove to be quite detrimental to the healthy individual, this lack of sleep and irregular schedule only exacerbates the presenting symptoms of this disease being that the individual is receives less time in our most deep and restful sleep stage which allows the body to replenish itself as well as to consolidate information. In recent years researchers have taken notice of this once overlooked facet of this disease, realizing that these sleep disturbances are often the first symptoms of this disease before the onset of any cognitive deficits.
Examining this disease through a lens which considers the influence of sleep as both a causal and predictive antecedent is ultimately an important step toward understanding the underlying causes of this disease as well as toward discovering potential protective factors. In addition to discovering future preventative measures for this disease, this research can also help individuals living with Alzheimer’s today as well as their families to live better lives now that we have an understanding of how insufficient sleep can exacerbate the other presenting symptoms of Alzheimer’s, patients and caregivers might find that certain lifestyle changes significantly improve their quality of life.
References:
Musiek, E. S., Xiong, D. D., & Holtzman, D. M. (2015). Sleep, circadian rhythms, and the pathogenesis of Alzheimer disease. Experimental & molecular medicine, 47(3), e148.
Early Treatment of Circadian Dysfunction for the Prevention of Alzheimer’s Disease
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