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The Sleeping Brain
Published in Hanno W. Kirk, Restoring the Brain, 2020
Research into brain activity during sleep has demonstrated that the so-called glymphatic system of the brain, analogous to the systemic lymphatic system of the body, probably acts as a conduit for flushing toxins from neurons into the general circulation. Putative neurotoxins, such as beta amyloid, alpha synuclein and tau, accumulate within the interstitium (ISF) of the CNS during consciousness. The ISF is in dynamic equilibrium with the cerebrospinal fluid (CSF), resulting in convective exchange between the two fluid compartments. The channels of the ISF, referred to as the glymphatic system, envelop the neurons, glia and cerebral vasculature with CSF influxing from the arterial side and ISF into the venules. During sleep, the volume of the glymphatic system increases by approximately 60% compared to waking, which allows for enhanced clearance of the aforementioned neurotoxins.13 The increase in clearance from this effective volume expansion is 95% compared to waking clearance. It may also be involved in neutralizing the soporific effects of adenosine that accumulates during consciousness.
What Actually Is Sleep?
Published in Zippi Dolev, Mordechai Zalesch, Judy Kupferman, Sleep and Women's Health, 2019
Zippi Dolev, Mordechai Zalesch, Judy Kupferman
The toxin clearance mechanism active during sleep is known as the “glymphatic system,” like the lymphatic system that clears toxic matter throughout the entire body. To date, the mechanism has been seen in mice and baboons; however, researchers have good reason to assume that the same process also occurs in human brains. One of the proteins that accumulates in the brain during the hours of daily activity is amyloid beta, known to cause Alzheimer's disease. Alzheimer's and other dementia diseases have also been found to be connected to sleep disorders. This has led scientists to assume that Alzheimer's and other neurological diseases are caused by unsatisfactory functioning of the toxin-cleansing process during sleep time. This can explain why we do not think clearly after a sleepless night, and why a lack of sleep over a period of time can cause death. So, if brain cleaning is a lifesaver, or at least a life preserver, why does it occur only during sleep? Why not perform toxin cleaning more frequently? Professor Nedergaard suggests that the cleansing process demands a huge amount of energy: “It is probably impossible for the brain to self-clean and at the same time to be aware of the surroundings, to talk, move, etc.”
Outdoor Air Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Regardless of the route, its solutes and proteins ultimately reach the liver, where they are degraded. As such, the glymphatic system, so named for its dependence on glial water channels and its adoption of a clearance function similar to that of the peripheral lymphatic system, avoids the need for local protein processing and degradation. Instead, it facilitates transport to the same central excretion and recycling sites used by other peripheral tissues.
Beyond the amyloid hypothesis: how current research implicates autoimmunity in Alzheimer’s disease pathogenesis
Published in Critical Reviews in Clinical Laboratory Sciences, 2023
Miyo K. Chatanaka, Dorsa Sohaei, Eleftherios P. Diamandis, Ioannis Prassas
The brain is a highly metabolic organ that accounts for 2% of human mass and 25% of glucose use [150]. When its soluble waste products are released into the brain’s interstitial spaces, where the interstitial fluid (ISF) resides, they are transported out of the CNS for degradation. The waste’s clearance happens through a CSF-ISF solute exchange, and this is facilitated by aquaporin 4 (AQP4) channels that decrease the resistance between the parenchymal perivascular and interstitial spaces [151]. Understanding the intricacies of solute drainage through the help of astrocytic AQP4 channels led to the naming of the pathway: glial-associated lymphatic system, or glymphatic system [151]. The glymphatic system, therefore, is a CNS-specific clearance system that allows for waste from the ISF to be drained out of the brain [152].
Phytochemical constituents and protective efficacy of Schefflera arboricola L. leaves extract against thioacetamide-induced hepatic encephalopathy in rats
Published in Biomarkers, 2022
Ali M. El-Hagrassi, Abeer F. Osman, Mostafa E. El-Naggar, Noha A. Mowaad, Sahar Khalil, Manal A. Hamed
Furthermore, TAA-induced hyperammonia was confirmed by the histopathological examination of TAA intoxicated brain tissue which revealed the classic pathophysiological structures of HE; such as obvious neuronal loss and neuronal degenerative changes especially in the cerebral cortex that appear as many shrunken darkly stained nuclei accompanied with perineuronal edema. This finding is inconsistent with prior studies of Mustafa et al. (2013) and Abdelaziz et al. (2015). These changes can be explained by the fact that ammonia can create free radicals, which reduce the antioxidant capacity of neurons and astrocytes. Ammonia also affects cells through a variety of mechanisms, including cellular swelling, inflammation, mitochondrial malfunction, cellular bioenergetics disruption, pH changes, and membrane potential changes. Furthermore, cirrhosis-related problems in the glymphatic system (a recently identified brain-wide pathway that promotes clearance of several toxic accumulating chemicals) have also been proposed as a possible explanation for brain dysfunction in people with liver cirrhosis (Hadjihambi et al. 2019).
Deciphering Alzheimer’s disease: predicting new therapeutic strategies via improved understanding of biology and pathogenesis
Published in Expert Opinion on Therapeutic Targets, 2020
Rita Khoury, George T. Grossberg
The glymphatic system has recently emerged as a new system of drug delivery to the brain that bypasses the BBB ‘gatekeeper’ of the CNS and decreased the risk of toxic peripheral side effects. For instance, insulin-like growth factor-1 (IGF-1) is a neuroprotective molecule that is associated with increased risk of carcinogenesis when administered peripherally. The ependymal route directly delivers IGF-1 to the brain at optimal concentrations and prevents any peripheral toxicity [62]. Additionally, AQP4 water channels is another therapeutic target within the glymphatic pathway. Unfortunately, no specific drug has yet been developed to target this molecule due to its poor druggability. AQP4 polarization at the astrocytic end-feet is however regulated by adenosine.Hence, developing selective blockers of Adenosine 2A receptors seems to be an interesting treatment strategy for AD [77].