摘要
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acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiologic agent of the 2019 coro-navirus disease (COVID-19), has affected more than 20 million people in Brazil and caused a global health emer-gency. This virus has the p...
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acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiologic agent of the 2019 coro-navirus disease (COVID-19), has affected more than 20 million people in Brazil and caused a global health emer-gency. This virus has the potential to affect various parts of the body and compromise metabolic functions. The virus-mediated neural inflammation of the nervous system is due to a storm of cytokines and oxidative stress, which are the clinical features of Alzheimer's disease (AD). This neurodegenerative disease is aggravated in cases involving SARS-CoV-2 and its inflammatory biomarkers, accelerating accumulation of b-amyloid peptide, hyperphosphorylation of tau protein, and production of reactive oxygen species, which lead to homeostasis imbalance. The cholinergic system, through neurons and the neurotransmitter acetylcholine (ACh), modulates various physiological pathways, such as the response to stress, sleep and wakefulness, sensory information, and the cognitive system. Patients with AD have low concentrations of ACh; hence, therapeutic methods are aimed at adjusting the ACh titers available to the body for maintaining functionality. Herein, we focused on acetyl -cholinesterase inhibitors, responsible for the degradation of ACh in the synaptic cleft, and muscarinic and nico-tinic receptor agonists of the cholinergic system owing to the therapeutic potential of the cholinergic anti-inflammatory pathway in AD associated with SARS-CoV-2 infection.(c) 2022 IBRO. Published by Elsevier Ltd. All rights reserved.
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