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Other postmortem surveys of three COVID-19 patients with severe symptoms showed that the cerebral cortex had increased numbers of reactive astrocytes and exacerbated microglial activation, as well as decreased glutathione levels and up-regulation of genes related to IL-1B, IL-6, interferon-inducible transmembrane, MX dynamin-like GTPase 1, and 2,5-oligoadenylate synthetase 2, suggesting a relationship between oxidative stress and neuroinflammation mediated by glia (Boroujeni et al

UCP1 is a proton channel which allows dissipation of the proton gradient across the mitochondrial matrix, without adenosine triphosphate (ATP) production