COVID-19中神经元和非神经元GABA:与精神病学的相关性

Pub Date : 2022-06-08 DOI:10.3390/reports5020022
A. Sfera, Karina G. Thomas, Sarvin Sasannia, Jonathan J. Anton, Christina V. Andronescu, Michael Garcia, Dan O. Sfera, M. Cummings, Z. Kozlakidis
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引用次数: 3

摘要

新冠肺炎大流行的病原体SARS-CoV-2的感染起源于中国,并迅速在全球传播。尽管经济和医疗保健遭受了巨大破坏,但对这种病毒的研究有助于更好地理解许多分子途径,包括涉及γ-氨基丁酸(GABA)的途径,这些途径将对后疫情时代的医学,包括神经精神病学产生积极影响。严重急性呼吸系统综合征冠状病毒2型主要通过肾素-血管紧张素系统的成分血管紧张素转化酶-2(ACE-2)进入宿主细胞。在其众多功能中,这种蛋白质上调GABA,不仅保护中枢神经系统,还保护内皮、胰腺和肠道微生物群。与ACE-2结合的严重急性呼吸系统综合征冠状病毒2篡夺了神经元和非神经元GABA能系统,导致神经精神疾病与肠道生态失调、内皮和代谢功能障碍的高度共病。在这篇前瞻性的文章中,我们仔细研究了病毒劫持非神经元GABA产生的病理学,并总结了恢复这些系统的潜在干预措施。
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Neuronal and Non-Neuronal GABA in COVID-19: Relevance for Psychiatry
Infection with SARS-CoV-2, the causative agent of the COVID-19 pandemic, originated in China and quickly spread across the globe. Despite tremendous economic and healthcare devastation, research on this virus has contributed to a better understanding of numerous molecular pathways, including those involving γ-aminobutyric acid (GABA), that will positively impact medical science, including neuropsychiatry, in the post-pandemic era. SARS-CoV-2 primarily enters the host cells through the renin–angiotensin system’s component named angiotensin-converting enzyme-2 (ACE-2). Among its many functions, this protein upregulates GABA, protecting not only the central nervous system but also the endothelia, the pancreas, and the gut microbiota. SARS-CoV-2 binding to ACE-2 usurps the neuronal and non-neuronal GABAergic systems, contributing to the high comorbidity of neuropsychiatric illness with gut dysbiosis and endothelial and metabolic dysfunctions. In this perspective article, we take a closer look at the pathology emerging from the viral hijacking of non-neuronal GABA and summarize potential interventions for restoring these systems.
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