However, in DSAD, additional astrocytes, such as ASC1 and ASC3 in the cortical upper layers, showed significant interactions mediated by ANGPTL4. Increased ANGPTL4 expression has been previously observed in astrocytes from patients with AD with vascular changes52, and co-immunofluorescence of ANGPTL4 and GFAP confirmed astrocytic ANGPTL4 upregulation in DSAD (two-way t test, P < 0.05; Fig. 6m,n). The gene discussed is GFAP; the disease is Alzheimer disease.