The COVID-19 pandemic has impacted virtually every aspect of human life, both socially and economically. While the immediate physical symptoms of the virus have been well-documented, the long-term effects are only now being studied. Recent research is highlighting the potential neurological effects that can manifest in patients long after they have recovered from COVID-19. This article explores the findings of a recent study regarding the potential long-term neurological effects post-COVID-19, shedding light on the important need for continued research into the impacts of the pandemic.
A new study published on the bioRxiv preprint server uses preclinical mouse models and human post-mortem samples to analyze the presence and distribution of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein in the skull-meninges-brain axis (SMB), including the recently discovered skull-meninges connection (SMC). The study aimed to understand the potential long-term neurological implications of COVID-19. The study revealed substantial accumulation of SARS-CoV-2 S protein in the niches of human skull marrow, meninges, SMC, and brain parenchyma in both mouse and human-origin samples. In healthy mice, direct microinjections of S into skull marrow niches triggered brain proteome alterations and parenchymal cell death. However, the observed accumulation of SARS-CoV-2 and its S glycoprotein at the CNS peripheries in the skull samples of some people suggested a likely mechanism for the neurological effects of SARS-CoV-2 infection. Studies have reported that SARS-CoV-2 S triggers the expression of inflammatory cytokines and chemokines in macrophages and lung epithelial cells, thereby compromising endothelial functions. In this study, it also activated an immune response in the SMB axis, potentially via recruiting and more neutrophils. Though the researchers could not distinguish the direct effects of S from the systemic effects of COVID-19. It acted as an inflammatory stimulus that led to the development of an immune response in the brain and increased the expression of pro-inflammatory proteins, e.g., calprotectin and pro-platelet basic protein. In the meninges, this inflammatory state led to the upregulation of neutrophil degranulation proteins. NETs triggered tissue damage, including endothelium damage, thereby altering coagulation processes and rationalizing why some COVID-19 patients develop mini-infarcts in the brain parenchyma. In fact, in the brain, proteins engaged in neurodegeneration pathways were highly dysregulated. Therefore, future investigations should focus on characterizing these proteins as biomarkers and therapeutic targets to prevent and treat COVID-19-related neuro-complications.
In conclusion, the study sheds light on the potential neurological effects that COVID-19 may have in the long-term. It emphasizes the importance of continued monitoring and research to better understand the impact of this virus on the brain and nervous system. As the world continues to grapple with the pandemic, it is crucial that we prioritize comprehensive care for those who have been infected with COVID-19, including monitoring and treatment for neurological symptoms. Only through increased understanding and collaboration can we effectively address the many challenges that the pandemic poses to our health and well-being.
