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Neuroinflammation and Oxidative Stress in the PCC Studies have shown that SARS-CoV-2 is neurotropic and neuroinvasive, disrupting the BBB to access brain tissue and initiating an inflammatory process that includes microglial activation, oxidative stress due to hypoxia, hypercoagulation, thrombosis, microbiome dysbiosis, accumulation of misfolded proteins, and neurological autoimmune responses which are considered principal events that induce mild neurological symptoms and headache and loss of smell to the most serious symptoms, such as stroke, encephalitis, infarctions, hemorrhagic lesions, and a hypercoagulable state [29,30,31,32]