Laboratory of Biological Chemistry of Neurodegenerative Disorders, Institute of Chemistry, Federal University of Rio de Janeiro, Rio de Janeiro 21941-909, Brazil.
ACS Chem Neurosci. 2020 Dec 16;11(24):4012-4016. doi: 10.1021/acschemneuro.0c00671. Epub 2020 Nov 27.
The current pandemic of coronavirus disease 2019 (COVID-19) has gained increased attention in the neuroscience community, especially taking into account the neuroinvasive potential of its causative agent, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and the impact of its infection on the structure and function of the brain. Apart from the neurotropic properties of SARS-CoV-2, it is likewise important the observation that virus infection may perturb specific cellular processes that are believed to play an important role in the pathogenesis of diverse neurological disorders, particularly in Parkinson's disease (PD). In this scenario, viral infection-induced colon inflammation, gut microbial imbalance, and α-synuclein upregulation are of particular interest with regard to the interplay between the gastrointestinal tract and the central nervous system (microbiome-gut-brain axis). In this Perspective, we present a critical view on the different hypotheses that are recently being raised by neuroscientists about the relationship between SARS-CoV-2 infection and long-lasting neurodegenerative disorders, opening the question of whether COVID-19 might represent a risk factor for the development of PD.
当前 2019 年冠状病毒病(COVID-19)大流行引起了神经科学界的高度关注,特别是考虑到其病原体严重急性呼吸系统综合征冠状病毒 2(SARS-CoV-2)的神经侵袭潜力,以及其感染对大脑结构和功能的影响。除了 SARS-CoV-2 的嗜神经性外,同样重要的是观察到病毒感染可能会扰乱特定的细胞过程,这些过程被认为在多种神经疾病的发病机制中起着重要作用,特别是在帕金森病(PD)中。在这种情况下,病毒感染引起的结肠炎症、肠道微生物失衡和α-突触核蛋白上调,与胃肠道和中枢神经系统(微生物群-肠道-大脑轴)之间的相互作用有关。在这篇观点文章中,我们对神经科学家最近提出的关于 SARS-CoV-2 感染与长期神经退行性疾病之间关系的不同假设进行了批判性的讨论,提出了 COVID-19 是否可能成为 PD 发病的一个风险因素的问题。
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