The Influence of SARS-CoV-2 Infection on the Development of Selected Neurological Diseases

Abstract

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.

Keywords: Alzheimer’s disease; CNS; COVID-19; SARS-CoV-2; ischemic stroke; multiple sclerosis; neuroinflammation.

Figure 1

Mechanism of the SARS-CoV-2 infection in Multiple Sclerosis. Captions: ACE2—angiotensin converting enzyme 2; SARS-CoV-2—severe acute respiratory syndrome coronavirus 2.

Figure 2

Mechanism of the SARS-CoV-2 infection in an ischemic stroke. Captions: ACE2—angiotensin converting enzyme 2; TNF-α—tumor necrosis factor α; IL—interleukin; NETs—neutrophil extracellular traps.

Figure 3

Mechanism of the SARS-CoV-2 infection in Alzheimer’s disease. Captions: Aβ/Aβ42—β amyloid plaques; ACE2—angiotensin converting enzyme 2; BDNF—brain-derived neurotrophic factor; NLRP3—NOD-, LRR- and pyrin domain-containing protein 3; ORF3a protein—open reading frame 3a protein.