The pathophysiology of neurological manifestations in COVID-19 is mechanistically diverse and includes direct neuroinvasion, immune dysregulation and systemic inflammation, hypoxic-ischemic processes, endothelial damage and microvascular injury, maladaptation of the angiotensin-converting enzyme (ACE2) pathway, and the unique psychosocial impacts of this infection and related pandemic [5,9]. This evidence concerns the gene ACE and infection.