Along with emergence of the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in late 2019, a myriad of neurologic symptoms, associated with structural brain changes, were reported. In this paper, we provide evidence to critically discuss the claim that the survived patients could possibly be at increased risk for neurodegenerative diseases via various mechanisms. This virus can directly invade the brain through olfactory bulb, retrograde axonal transport from peripheral nerve endings, or via hematogenous or lymphatic routes. Infection of the neurons along with peripheral leukocytes activation results in pro-inflammatory cytokine increment, rendering the brain to neurodegenerative changes. Also, occupation of the angiotensin-converting enzyme 2 (ACE-2) with the virus may lead to a decline in ACE-2 activity, which acts as a neuroprotective factor. Furthermore, acute respiratory distress syndrome (ARDS) and septicemia induce hypoxemia and hypoperfusion, which are locally exacerbated due to the hypercoagulable state and micro-thrombosis in brain vessels, leading to oxidative stress and neurodegeneration. Common risk factors for COVID-19 and neurodegenerative diseases, such as metabolic risk factors, genetic predispositions, and even gut microbiota dysbiosis, can contribute to higher occurrence of neurodegenerative diseases in COVID-19 survivors. However, it should be considered that severity of the infection, the extent of neurologic symptoms, and the persistence of viral infection consequences are major determinants of this association. Importantly, whether this pandemic will increase the overall incidence of neurodegeneration is not clear, as a high percentage of patients with severe form of COVID-19 might probably not survive enough to develop neurodegenerative diseases.

随着 2019 年底新型严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 的出现，报告了与大脑结构变化相关的无数神经系统症状。在本文中，我们提供证据来批判性地讨论幸存的患者可能通过各种机制增加患神经退行性疾病的风险这一说法。这种病毒可以通过嗅球直接侵入大脑，从周围神经末梢逆行轴突运输，或通过血行或淋巴途径。神经元的感染以及外周白细胞的激活导致促炎细胞因子增加，使大脑发生神经退行性变化。此外，血管紧张素转换酶 2 (ACE-2) 被病毒占据可能导致 ACE-2 活性下降，它作为一种神经保护因子。此外，急性呼吸窘迫综合征（ARDS）和败血症会引起低氧血症和低灌注，由于脑血管中的高凝状态和微血栓形成而局部加剧，导致氧化应激和神经变性。COVID-19 和神经退行性疾病的常见风险因素，例如代谢风险因素、遗传易感性，甚至肠道微生物群失调，都可能导致 COVID-19 幸存者神经退行性疾病的发生率更高。然而，应该考虑到感染的严重程度、神经系统症状的程度和病毒感染后果的持续性是这种关联的主要决定因素。重要的是，这种流行病是否会增加神经退行性疾病的总体发病率尚不清楚，