Neurological manifestations in COVID-19 patients can be mediated via multiple mechanisms, including viral neurotropism, cerebral hypoxia provoked by respiratory failure, or an immune-mediated mechanism through a cytokine storm, acting via angiotensin-converting enzyme 2 (ACE-2) receptors with subsequent endothelial dysfunction [8,9,12,16]. Here, ACE2 is linked to endothelial dysfunction.