While literature concerning the presence and effect of GFAP-positive reactive astrogliosis in humans with AD remains largely incohesive, studies performed in disease models have shown that experimentally attenuating reactive astrocyte proliferation results in the advancement of Aβ pathology [89], highlighting our observation of chronically reduced GFAP-positive astrocytes in COVID patients as a potential avenue for AD advancement. Here, GFAP is linked to Alzheimer disease.