Interestingly, the SARS-CoV-2 infection seems to instigate and/or accelerate the AD phenotype by inhibiting ACE2 enzymatic activity, triggering a hyperinflammatory response and downregulating the secretion of BDNF, a potent neurotrophin endowed with crucial functions in supporting neurogenesis, cognition and the prevention of neurodegeneration upon binding to its cognate transmembrane TrkB receptor protein [117]. Here, ACE2 is linked to Alzheimer disease.