Cytokine storm and neuropathological alterations in patients with neurological manifestations of COVID-19.

The COVID-19 pandemic is caused by the severe acute respiratory syndrome coronavirus (SARS-CoV-2), a respiratory pathogen with neuroinvasive potential. Neurological COVID-19 manifestations include loss of smell and taste, headache, dizziness, stroke, and potentially fatal encephalitis. Several studies found elevated proinflammatory cytokines such as TNF-α, IFN-γ, IL-6 IL-8, IL-10 IL-16, IL-17A, and IL-18 in severely and critically ill COVID-19 patients, which may persist even after apparent recovery from infection. Biomarker studies on CSF and plasma and serum from COVID-19 patients have also shown a high level of IL-6, intrathecal IgG, neurofilament light chain (NFL), glial fibrillary acidic protein (GFAP), and tau protein. Emerging evidence on the matter has established the concept of COVID-19 associated neuroinflammation, in the context of COVID-19 associated cytokine storm. While the short-term implications of this condition are extensively documented, its long-term implications are yet to be understood. The association of the aforementioned cytokines with the pathogenesis of neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, Huntington disease, and amyotrophic lateral sclerosis, may increase COVID-19 patients' risk to develop neurodegenerative diseases. Analysis of proinflammatory cytokines and CSF biomarkers in patients with COVID-19 can contribute to the early detection of the disease's exacerbation, monitoring the neurological implications of the disease and devising risk scales, and identifying treatment targets.

Efficacy of the current investigational drugs for the treatment of COVID-19: a scoping review.

To date, there is no final FDA-approved treatment for COVID-19. There are thousands of studies published on the available treatments for COVID-19 virus in the past year. Therefore, it is crucial to synthesize and summarize the evidence from published studies on the safety and efficacy of experimental treatments of COVID-19. We conducted a systematic literature search of MEDLINE, PubMed, Cochrane Library, GHL, OpenGrey, ICTRP, and ClinicalTrials.gov databases through April 2020. We obtained 2699 studies from the initial literature search. Of them, we included 28 eligible studies that met our eligibility criteria. The sample size of the included studies is 2079 individuals. We extracted and pooled the available data and conducted a quality assessment for the eligible studies. From the 28 studies, only 13 studies provide strong evidence. Our results showed that Favipiravir and Hydroxycholoroquine shorten viral clearance and clinical recovery time and promote pneumonia absorption. On the other hand, Lopinavir-ritonavir either alone or combined with arbidol or interferons has no significant difference superior to the standard care. Corticosteroids, Convalescent plasma transfusion, and anticoagulant therapies provide a better prognosis. Remedsivir, Tocilizumab, Immunoglobulin, Mesenchymal stem cell transplantation showed effective treatment results, but further confirmatory studies are needed. In conclusion, Favipiravir and Remedsivir might be promising drugs in the treatment of COVID-19 patients. .