Compelling studies have shown that COVID-19 and AD share several physiopathological aspects including ACE2 expression, age, inflammation with “cytokine storm”, oxidative stress, the APOE4 genetic variant, the neurotransmitter system, hypoxia and the activation of intracellular pathways associated with the altered metabolism of APP/Aβ and tau (Figure 4). This evidence concerns the gene APP and Alzheimer disease.