Abstract
The SARS-CoV-2 virus that resulted in the COVID-19 pandemic has been implicated in a range of neurological issues, such as encephalopathy, stroke, and cognitive decline. Although the precise mechanism causing these issues is unknown, mounting evidence shows that blood-brain barrier (BBB) disruption is probable2 a major factor. The integrity of the blood-brain barrier (BBB), a highly selective barrier that divides the brain from the systemic circulation, is crucial for preserving normal brain function. By analysing the multi-transcriptome data, this work explores the neurological impacts of the SARS-CoV-2 virus and provides insight into the molecular mechanisms behind BBB breakdown and neurological symptoms in COVID-19 patients. The endothelial cells of BBB expresses inflammatory genes in response to the systemic inflammation induced due to SARS-CoV-2 remnants in the body. This raises the possibility that systemic inflammation brought on by SARS-CoV-2 and BBB integrity are correlated. Furthermore, the study highlights the pathways involved in oxidative stress and endothelial cell activation, revealing their role in COVID-19 passage through BBB and induction of systemic inflammation and advancement toward neurological disorders. The article showcases the evidence that mitochondrial dysfunction is a major aftermath associated with SARS-CoV-2 infection as the impaired Mitochondria leads to an accumulation of reactive oxygen species (ROS), triggering endothelial dysfunction, and leading to the passage of harmful molecules across the BBB. This study offers insightful information that may open up the possibilities for new treatment plans by targeting biomarkers specifically associated with inflammation and BBB dysfunctioning conditions.