Possible mechanisms include immunosenescence, heightened IFN responses or genetic predisposition to severe COVID-19 (OAS1, APOE ε4 allele) in Alzheimer’s disease [350,408,409,410], respiratory muscle rigidity and insufficient cough reflex in Parkinson’s disease [350,411], systemic inflammation in epilepsy (with much uncertainty) [362,412] and susceptibility to acute stress in cerebrovascular diseases [413,414]. This evidence concerns the gene IFNA1 and COVID-19.