by Nanda Nayak
Whether it be the constant complaints about exhaustion from students around campus or our own sleep-deprivation, it seems like no one ever gets enough sleep. Sleep-deprivation has long been associated with short-term inattentiveness and decreased memory retainment, but there appears to be a more severe negative ramification: association with Alzheimer’s disease.
Alzheimer’s disease is a progressive neurodegenerative disorder that leads to cognitive impairment and memory loss. Alzheimer’s affected about 46.8 million people in 2015, and is projected to impact about 131.5 million people by 2050. With its ever-growing prevalence and consequential medical implications, Alzheimer’s disease represents a serious medical threat that researchers and health professionals alike are striving to mitigate.
And it seems like one easy solution might come in the form of simply getting enough sleep.
To really understand the connection between sleep and Alzheimer’s disease, we must first examine biological macromolecules at a neuronal level.
Beta-amyloid (Aβ) protein and tau protein are neuronal proteins found in the intracellular and cerebrospinal fluid in the nervous system. While both Aβ protein and tau protein are found in a normal functioning brain, they are associated with a series of pathological diseases called “tauopathies,” (of which Alzheimer’s Disease is an example) in which phosphorylated tau proteins and Aβ protein aggregate into clusters that begin to proliferate across the brain. The presence and dispersion of Aβ and tau protein clusters has been strongly correlated with loss of neuronal function, synaptic junction disruptions, and impairment of cognitive performance.
How does this all relate to sleep? The glymphatic system is an organ system that primarily serves to remove protein macromolecules, including Aβ protein and tau protein, from the central nervous system. Because the glymphatic system is more active during sleep, sleep deprivation negatively impacts the clearance of these proteins and leads to higher levels of protein aggregation. Chronic sleep deprivation in humans was correlated with a 50% increase in tau protein clusters and a 30% increase in Aβ protein clusters in the cerebrospinal fluid (Holth et al., 2019). In addition, chronic sleep deprivation is also correlated with the spread of these tau pathological clusters over different parts of the brain.
Thus, getting enough sleep may have a warding effect on the toxic build-up of Aβ and tau protein in the brain, and can serve as a measure in tauopathy prevention. Sleep treatments to promote the delaying of Alzheimer’s are currently under investigation, and are implemented as a treatment for Parkinson’s disease, another neurological disorder.
To the rest of us, the implications are clear: this is just another reason supporting the benefits and importance of sleep, and we should all make an active effort to ensure we are getting enough of it.
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