[SARS-CoV-2 (COVID-19) as a predictor of neuroinflammation and neurodegeneration: potential therapy strategies].
M V PutilinaD V GrishinPublished in: Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova (2020)
The pandemic caused by the SARS-CoV-2 virus (COVID-19) made it necessary to evaluate in more detail the processes of neuroinflammation as an integral component of the pathogenesis of viral infection. The acute neuroinflammatory response includes the activation of resident tissue macrophages in the CNS and the subsequent release of various cytokines and chemokines, which probably activates oxidative stress, causing long-term neuronal damage. This makes urgent the search for drugs with indirect anti-inflammatory effects with proven effectiveness. From this point of view, it is worth further studying the treatment of patients with COVID-19 with dipyridamole, which, with its antiviral activity and anti-inflammatory effect, inhibiting acute inflammation and progressive fibrosis, is the drug of choice, especially for patients with early signs of elevated D-dimer concentrations and pronounced clinical symptoms of microangiopathy.
Keyphrases
- sars cov
- oxidative stress
- liver failure
- drug induced
- respiratory syndrome coronavirus
- respiratory failure
- lipopolysaccharide induced
- anti inflammatory
- cerebral ischemia
- traumatic brain injury
- coronavirus disease
- randomized controlled trial
- aortic dissection
- lps induced
- dna damage
- multiple sclerosis
- cognitive impairment
- systematic review
- diabetic rats
- ischemia reperfusion injury
- hepatitis b virus
- stem cells
- patient safety
- inflammatory response
- depressive symptoms
- emergency department
- bone marrow
- physical activity
- risk assessment
- extracorporeal membrane oxygenation
- brain injury
- subarachnoid hemorrhage
- climate change
- cell therapy
- human health
- smoking cessation
- emergency medicine