ST18, and the overview of intersection set sizes in Suppl. Fig. S5). The well-established AD risk factor gene Apoe displayed sex-neutral microglial over-expression in both the 7 month and 17 months THY-Tau22 datasets. Finally, Malat1’s alteration patterns also extended beyond oligodendrocytes, e.g., showing consistent underexpression in astrocytes and OPCs as well, suggesting its broad involvement in multiple cell types relevant to AD pathology. The gene discussed is MALAT1; the disease is Alzheimer disease.