推测 COVID-19 与亨廷顿氏病之间的分子相互联系

IF 0.3 Q4 MEDICINE, RESEARCH & EXPERIMENTAL
Duygu SARI AK, Omar Alomari, Ülkan Kılıç
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引用次数: 0

摘要

目的:由于 2019 年冠状病毒病(COVID-19)大流行,全球医疗保健系统面临着前所未有的挑战。虽然呼吸道疾病是 COVID-19 最常见的症状,但越来越多的证据表明该病毒会造成神经系统损伤。为了指导疾病的临床治疗,必须阐明 COVID-19 的病理生理学机制。多项研究表明,COVID-19 患者的脑源性神经营养因子(BDNF)水平降低,而这也是亨廷顿病(一种神经退行性疾病)的特征之一。本研究的目的是调查 COVID-19 与亨廷顿病之间可能存在的联系。这一目的是为了指导 COVID-19 的临床治疗,尤其是考虑到越来越多的证据表明该病毒造成了神经损伤,包括 BDNF 水平的降低,而 BDNF 也是亨廷顿病的特征之一。研究方法对 COVID-19 和亨廷顿氏病进行全面的文献综述,重点研究与这两种疾病相关的基因。然后使用 STRING 数据库对这些基因进行分析,确定蛋白质之间的相互作用,旨在阐明 COVID-19 的病理生理学机制及其与亨廷顿病的潜在联系。研究结果研究结果表明,根据文献研究和 STRING 数据库分析,COVID-19 与亨廷顿氏病之间可能存在分子水平的相互作用。虽然这些相互作用背后的主要机制尚未完全明了,但假设表明,BDNF 及其高亲和力受体 TrkB 可能发挥了关键作用。此外,该研究还强调嗅觉功能障碍是 COVID-19 的常见症状,这也与包括亨廷顿氏病在内的多种神经退行性疾病有关。结论这项研究强调了 COVID-19 与神经退行性疾病之间的联系,特别是通过嗅觉功能障碍这一 COVID-19 与亨廷顿氏病的共同症状。观察到的潜在分子相互作用表明,COVID-19 可能会加剧神经退行性过程。这强调了进一步研究嗅觉功能障碍这一关键症状的迫切需要,以便更好地了解和管理 COVID-19 对神经退行性疾病患者的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Presumptive Molecular Interconnections Between COVID-19 And Huntington’s Disease
Objective: The healthcare system worldwide has faced unparalleled challenges as a result of the coronavirus disease of 2019 (COVID-19) pandemic. While respiratory tract disease is the most common symptom of COVID-19, there is increasing evidence of neurological damage caused by the virus. To guide the clinical management of the disease, it is essential to elucidate the mechanisms underlying the pathophysiology of COVID-19. Various research indicate that COVID-19 patients exhibit reduced levels of brain-derived neurotrophic factor (BDNF), which is also a hallmark of Huntington’s disease, a neurodegenerative disorder. The objective of this study is to investigate the possible links between COVID-19 and Huntington’s disease. This aim is motivated by the need to guide the clinical management of COVID-19, especially given the increasing evidence of neurological damage caused by the virus, including reduced levels of BDNF, a hallmark also observed in Huntington’s disease. Methods: The comprehensive literature review conducted for both COVID-19 and Huntington’s disease, focusing on the genes associated with both conditions. These genes were then analyzed using the STRING database to determine protein-protein interactions, aiming to elucidate the mechanisms underlying the pathophysiology of COVID-19 and its potential connections to Huntington’s disease. Results: The outcomes of the study indicate that there could be molecular-level interactions between COVID-19 and Huntington’s disease, based on the literature research and STRING database analysis. Although the primary mechanism behind these interactions is not yet fully understood, the hypothesis suggests that BDNF and its high-affinity receptor TrkB may play a crucial role. Additionally, the study highlights olfactory dysfunction as a common symptom of COVID-19, which is also linked with various neurodegenerative conditions, including Huntington’s disease. Conclusion: This work emphasizes the connection between COVID-19 and neurodegenerative diseases, particularly through the lens of olfactory dysfunction, a common symptom shared by COVID-19 and Huntington’s disease. The potential molecular interactions observed suggest that COVID-19 could exacerbate neurodegenerative processes. This underscores the critical need for further research focused on olfactory dysfunction as a key symptom, to better understand and manage the implications of COVID-19 in patients with neurodegenerative conditions.
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Clinical and Experimental Health Sciences
Clinical and Experimental Health Sciences MEDICINE, RESEARCH & EXPERIMENTAL-
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