Inflammatory Response Leads to Neuronal Death in Human Post-Mortem Cerebral Cortex in Patients with COVID-19.
Mahdi Eskandarian BoroujeniLeila SimaniHans A R BluyssenHamid Reza SamadikhahSoheila Zamanlui BenisiSanaz HassaniNader Akbari DilmaghaniMobina FathiKimia VakiliGholam-Reza MahmoudiaslHojjat Allah AbbaszadehMeysam Hassani MoghaddamMohammad-Amin AbdollhifarAbbas AghaeiPublished in: ACS chemical neuroscience (2021)
The recent coronavirus disease of 2019 (COVID-19) pandemic has adversely affected people worldwide. A growing body of literature suggests the neurological complications and manifestations in response to COVID-19 infection. Herein, we explored the inflammatory and immune responses in the post-mortem cerebral cortex of patients with severe COVID-19. The participants comprised three patients diagnosed with severe COVID-19 from March 26, 2020, to April 17, 2020, and three control patients. Our findings demonstrated a surge in the number of reactive astrocytes and activated microglia, as well as low levels of glutathione along with the upregulation of inflammation- and immune-related genes IL1B, IL6, IFITM, MX1, and OAS2 in the COVID-19 group. Overall, the data imply that oxidative stress may invoke a glial-mediated neuroinflammation, which ultimately leads to neuronal cell death in the cerebral cortex of COVID-19 patients.
Keyphrases
- coronavirus disease
- oxidative stress
- sars cov
- inflammatory response
- end stage renal disease
- cell death
- cerebral ischemia
- immune response
- subarachnoid hemorrhage
- ejection fraction
- newly diagnosed
- endothelial cells
- chronic kidney disease
- prognostic factors
- functional connectivity
- respiratory syndrome coronavirus
- brain injury
- peritoneal dialysis
- dendritic cells
- lps induced
- lipopolysaccharide induced
- patient reported outcomes
- machine learning
- patient reported
- cell proliferation
- long non coding rna
- dna damage
- big data
- artificial intelligence
- risk factors
- endoplasmic reticulum stress
- electronic health record
- induced apoptosis
- pi k akt
- heat shock