Flush it Out: The Role of Sleep in Removing Wastes in the Brain
Sleep is a broadly conserved function that is present across a variety of species. Since no species has been able to completely eliminate the need for sleep, there is strong evidence that sleep is playing an essential role that is critical for survival. One potential explanation for sleep is its role in metabolic homeostasis. Nearly all biological activity results in the production of metabolic waste products. This accumulation of wastes in the brain could cause disruptions in neuronal signaling and result in neuronal injury. Therefore, it is likely that sleep plays a role in removing toxic wastes from the brain to maintain its normal function.
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Although there have been hypotheses that sleep could be acting as a window for the brain to remove wastes, the mechanism had yet to be elucidated. In a study done by Lulu Xie and others at the University of Rochester Medical Center, the cerebrospinal fluid (CSF) influx, the volume of the interstitial space, and the rate of beta-amyloid clearance were examined in mice who were either awake, naturally asleep, or under anesthesia in order to investigate the mechanism behind this sleep-induced waste clearance. The glymphatic system is a process in which CSF interchanges with interstitial fluid (ISF) to remove wastes products. In order to investigate the differences in this process between awake and sleeping mice, a fluorescent tracer was injected to measure CSF movement. The results showed that CSF influx was reduced in awake animals as compared to sleeping or anesthetized animals. Since CSF flow was increased in sleeping animals, this suggests that the brain could be removing wastes via CSF. Furthermore, the volume of the interstitial space was found to be smaller in awake animals. The increase in the volume of the interstitial space during sleep would allow for more efficient clearance of wastes from the brain, and thus could be a key factor in this process. In order to track the removal of wastes, beta-amyloids, which are peptides that typically accumulate and form plaques characteristic in Alzheimer’s disease, were studied. The formation of these beta-amyloid plaques are thought to be involved in the cognitive deterioration in Alzheimer’s patients. Therefore, the proper removal of beta-amyloid appears to be essential to normal brain function. The clearance of beta-amyloid was examined by injecting radiolabeled beta-amyloid in the mice. The brains were then collected and analyzed for the amount of beta-amyloid remaining. Beta-amyloid clearance appeared to be faster in sleeping animals than in awake animals, with there being no difference in clearance seen between sleeping and anesthetized animals. In order to elucidate a possible mechanism behind the differences in interstitial space volume, the researchers examined noradrenaline activity in these animals. When the adrenergic receptor, the target of action of adrenaline, was blocked in animals, there was an increase in interstitial volume that was similar to the increase seen in sleeping or anesthetized animals, which suggests the role of adrenergic signaling in metabolic wastes clearance.
These findings have strong implications for the important role of sleep in toxic waste clearance in the brain. Toxic wastes that concentrate in the brain have significant negative impacts on the overall function of the brain and possibly could be implicated in certain diseases. For examples, the accumulation of beta-amyloid is a key marker in Alzheimer’s, and the presence of other proteins in the interstitial space of the brain have been linked to other neurodegenerative diseases. Sleep could be playing a key regulatory role in these diseases and further investigation into this area could further elucidate this critical link.
These findings have strong implications for the important role of sleep in toxic waste clearance in the brain. Toxic wastes that concentrate in the brain have significant negative impacts on the overall function of the brain and possibly could be implicated in certain diseases. For examples, the accumulation of beta-amyloid is a key marker in Alzheimer’s, and the presence of other proteins in the interstitial space of the brain have been linked to other neurodegenerative diseases. Sleep could be playing a key regulatory role in these diseases and further investigation into this area could further elucidate this critical link.
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