Department of Biochemical Diagnostics, Medical University of Bialystok, Waszyngtona 15A St., 15-269 Bialystok, Poland.
Department of Neurodegeneration Diagnostics, Medical University of Bialystok, Waszyngtona 15A St., 15-269 Bialystok, Poland.
Int J Mol Sci. 2024 Aug 9;25(16):8715. doi: 10.3390/ijms25168715.
In 2024, over 775 million cases of COVID-19 were recorded, including approximately 7 million deaths, indicating its widespread and dangerous nature. The disease is caused by the SARS-CoV-2 virus, which can manifest a wide spectrum of symptoms, from mild infection to respiratory failure and even death. Neurological symptoms, such as headaches, confusion, and impaired consciousness, have also been reported in some COVID-19 patients. These observations suggest the potential of SARS-CoV-2 to invade the central nervous system and induce neuroinflammation during infection. This review specifically explores the relationship between SARS-CoV-2 infection and selected neurological diseases such as multiple sclerosis (MS), ischemic stroke (IS), and Alzheimer's disease (AD). It has been observed that the SARS-CoV-2 virus increases the production of cytokines whose action can cause the destruction of the myelin sheaths of nerve cells. Subsequently, the body may synthesize autoantibodies that attack nerve cells, resulting in damage to the brain's anatomical elements, potentially contributing to the onset of multiple sclerosis. Additionally, SARS-CoV-2 exacerbates inflammation, worsening the clinical condition in individuals already suffering from MS. Moreover, the secretion of pro-inflammatory cytokines may lead to an escalation in blood clot formation, which can result in thrombosis, obstructing blood flow to the brain and precipitating an ischemic stroke. AD is characterized by intense inflammation and heightened oxidative stress, both of which are exacerbated during SARS-CoV-2 infection. It has been observed that the SARS-CoV-2 demonstrates enhanced cell entry in the presence of both the ACE2 receptor, which is already elevated in AD and the ApoE ε4 allele. Consequently, the condition worsens and progresses more rapidly, increasing the mortality rate among AD patients. The above information underscores the numerous connections between SARS-CoV-2 infection and neurological diseases.
2024 年,记录了超过 7.75 亿例 COVID-19 病例,其中约有 700 万人死亡,这表明其具有广泛而危险的性质。该疾病是由 SARS-CoV-2 病毒引起的,它可以表现出广泛的症状,从轻症感染到呼吸衰竭,甚至死亡。一些 COVID-19 患者还出现了头痛、意识混乱和意识障碍等神经系统症状。这些观察结果表明,SARS-CoV-2 有可能在感染期间入侵中枢神经系统并引发神经炎症。本综述特别探讨了 SARS-CoV-2 感染与多发性硬化症(MS)、缺血性中风(IS)和阿尔茨海默病(AD)等选定神经系统疾病之间的关系。已经观察到,SARS-CoV-2 病毒会增加细胞因子的产生,其作用会导致神经细胞的髓鞘破坏。随后,身体可能会合成攻击神经细胞的自身抗体,导致大脑解剖元素受损,从而可能导致多发性硬化症的发作。此外,SARS-CoV-2 会加剧炎症,使已经患有 MS 的患者的病情恶化。此外,促炎细胞因子的分泌可能导致血栓形成加剧,从而导致血栓形成,阻塞大脑的血液流动并引发缺血性中风。AD 的特征是强烈的炎症和氧化应激增加,这两者在 SARS-CoV-2 感染期间都会加剧。已经观察到,SARS-CoV-2 在 ACE2 受体(AD 中已经升高)和 ApoE ε4 等位基因存在的情况下,增强了细胞进入。因此,病情恶化并更快地进展,增加了 AD 患者的死亡率。上述信息强调了 SARS-CoV-2 感染与神经系统疾病之间的许多联系。