Chair and Department of Family Medicine, Medical University of Lublin, Langiewicza 6a, 20-035 Lublin, Poland.
Student Scientific Society, Chair and Department of Family Medicine, Medical University of Lublin, Langiewicza 6a, 20-035 Lublin, Poland.
Int J Environ Res Public Health. 2023 Jan 25;20(3):2146. doi: 10.3390/ijerph20032146.
Alzheimer's disease (AD) is a life-changing condition whose etiology is explained by several hypotheses. Recently, a new virus contributed to the evidence of viral involvement in AD: the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes the COVID-19 coronavirus disease. AD was found to be one of the most common COVID-19 comorbidities, and it was found to increase mortality from this disease as well. Moreover, AD patients were observed to present with the distinct clinical features of COVID-19, with delirium being prevalent in this group. The SARS-CoV-2 virus enters host cells through the angiotensin-converting enzyme 2 (ACE2) receptor. ACE2 is overexpressed in brains with AD, which thus increases the viral invasion. Furthermore, the inhibition of the ACE2 receptor by the SARS-CoV-2 virus may also decrease the brain-derived neurotrophic factor (BDNF), contributing to neurodegeneration. The ApoE ε4 allele, which increases the risk of AD, was found to facilitate the SARS-CoV-2 entry into cells. Furthermore, the neuroinflammation and oxidative stress existing in AD patients enhance the inflammatory response associated with COVID-19. Moreover, pandemic and associated social distancing measures negatively affected the mental health, cognitive function, and neuro-psychiatric symptoms of AD patients. This review comprehensively covers the links between COVID-19 and Alzheimer's disease, including clinical presentation, molecular mechanisms, and the effects of social distancing.
阿尔茨海默病（AD）是一种改变生活的疾病，其病因可以用几种假说来解释。最近，一种新病毒为病毒在 AD 中的作用提供了新的证据：引起 COVID-19 冠状病毒病的严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）。AD 被发现是 COVID-19 最常见的合并症之一，而且这种疾病的死亡率也有所增加。此外，AD 患者表现出 COVID-19 的明显临床特征，其中谵妄很常见。SARS-CoV-2 病毒通过血管紧张素转换酶 2（ACE2）受体进入宿主细胞。AD 大脑中 ACE2 表达过度，从而增加了病毒的入侵。此外，SARS-CoV-2 病毒对 ACE2 受体的抑制也可能降低脑源性神经营养因子（BDNF），导致神经退行性变。增加 AD 风险的 ApoE ε4 等位基因被发现有助于 SARS-CoV-2 进入细胞。此外，AD 患者存在的神经炎症和氧化应激会增强与 COVID-19 相关的炎症反应。此外，大流行及其相关的社会隔离措施对 AD 患者的心理健康、认知功能和神经精神症状产生了负面影响。本综述全面涵盖了 COVID-19 与阿尔茨海默病之间的联系，包括临床表现、分子机制以及社会隔离的影响。
