According to recent data, several mechanisms of viral invasion of the central nervous system (CNS) have been proposed, one of which is both direct penetration of the virus through afferent nerve fibers and damage to the endothelium of cerebral vessels. It has been proven that the SARS-CoV-2 virus affects pathologically not only the human cardiorespiratory system but is also associated with a wide range of neurological diseases, cerebrovascular accidents, and neuromuscular pathologies. However, the observed post-COVID symptom complex in patients, manifested in the form of headache, "fog in the head," high temperature, muscle weakness, lowering blood pressure, does it make us think about the pathophysiological mechanisms that contribute to the development of this clinical picture? One possible explanation is a disruption in the signaling of the acetylcholine system (AChS) in the body. Viral invasions, and in particular COVID-19, can negatively affect the work of the AChS, disrupting its coordination activities. Therefore, the main goal of this literature review is to analyze the information and substantiate the possible mechanisms for the occurrence of post-COVID syndrome in people who have had COVID-19 from the standpoint of AChS dysfunctions.
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http://dx.doi.org/10.4103/cjop.CJOP-D-22-00072 | DOI Listing |
Molecules
December 2024
Ufa Institute of Chemistry, Ufa Federal Research Centre, Russian Academy of Science, 71, Prospect Octyabrya, Ufa 450054, Russia.
Alzheimer's disease (AD) poses a significant public health issue. Despite the fact that today there are several methods of maintenance therapy, one of the most widely used methods is designed to correct the deficiency of acetylcholine. In the search for new potential inhibitors of cholinesterase enzymes, eight new derivatives of 3-oxo- or 2,3-indolo-triterpenic acid conjugated with amino-quinuclidine bicyclic cores were designed and synthesized.
View Article and Find Full Text PDFCell Biochem Biophys
January 2025
Department of Rehabilitation Therapeutics, School of Nursing, Jilin University, Changchun, Jilin, China.
Cholinergic deficiency and neuroinflammation are the two main factors of Alzheimer's disease. Recent studies have shown that water-soluble ginseng oligosaccharides (WGOS) derived from Panax ginseng roots can protect against scopolamine-induced impairments in learning and memory. However, the fundamental mechanisms remain unclear for the most part.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Department of Anesthesiology and Critical Care Medicine, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin, China; Tianjin Key Laboratory of Acute Abdomen Disease Associated Organ Injury and ITCWM Repair, Tianjin Nankai Hospital, Tianjin, China. Electronic address:
During the process of acute lung injury (ALI) associated with sepsis, the α7nAChR in the cholinergic anti-inflammatory pathway (CAP) plays a crucial role. However, the roles of electroacupuncture (EA) and specialized pro-resolving mediators (SPMs) in this context remain unclear. In this study, we demonstrated that EA activates CAP via α7nAChR, reducing lung permeability and inflammatory cytokine release.
View Article and Find Full Text PDFJ Physiol
January 2025
Université Paris Cité, CNRS, ENS Paris Saclay, Centre Borelli UMR 9010, Paris, France.
Terminal Schwann cells (TSCs) are capable of regulating acetylcholine (ACh) release at the neuromuscular junction (NMJ). We have identified GABA as a gliotransmitter at mouse NMJs. When ACh activates α7 nicotinic ACh receptor (nAChRs) on TSCs, GABA is released and activates GABA receptors on the nerve terminal that subsequently reduce ACh release.
View Article and Find Full Text PDFInt J Biol Macromol
January 2025
State Key Laboratory of Subtropical Silviculture, Zhejiang A & F University, Hangzhou 311300, PR China; College of Food and Health, Zhejiang A & F University, Hangzhou 311300, PR China. Electronic address:
Aberrant autophagic flux and epigenetic mechanisms are involved in the development of neurodegenerative diseases. However, limited studies have been conducted on the relationship between the histone acetylation-particularly sirtuin 2 (SIRT2)-and autophagy in cognitive deficiency. We investigated the effects of a walnut-derived peptide (WNP-8) on SIRT2, synaptic plasticity, and autophagy and the involvement of SIRT2 in learning and memory.
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