In aged mice, Atg7 deficiency in microglia impacts UPR and oxidative stress but not microglia numbers. (A) Immunoblots for ATG7 and p62 proteins in microglial lysates. Actin was assessed as a loading control. Microglia were sorted from 20-mo-old Atg7^fl/fl and Atg7^ΔMG mice. Experiments were repeated with three biological replicates. (B) Left: Representative confocal images from the cortex of 20-mo-old Atg7^fl/fl and Atg7^ΔMG mice showing the distribution of IBA1⁺ microglia (orange). Scale bar = 100 μm. Right: Quantification of microglia density in the cortex and hippocampus of 20-mo-old Atg7^fl/fl and Atg7^ΔMG mice. Each data point represents one mouse with four technical repeats. ns = not significant by unpaired t test. Data are presented as mean ± SEM. (C) Heatmap showing the genes differentially expressed in aged Atg7^fl/fl and Atg7^ΔMG microglia, detected by bulk RNA-seq. N = 3 for each genotype. (D) GO term analysis for genes upregulated in microglia from Atg7^fl/fl (upper panel) and Atg7^ΔMG mice (lower panel). (E) Venn diagram showing the number of DEGs shared by these comparisons: Atg7^fl/fl versus Atg7^ΔMG HM (HM-nonAD); Atg7^fl/fl-5xFAD versus Atg7^ΔMG-5xFAD mice HM (HM-AD); Atg7^fl/fl-5xFAD versus Atg7^ΔMG-5xFAD mice DAM and TM (DAM and TM-AD); and microglia from 20-mo-old Atg7^fl/fl and Atg7^ΔMG mice (Aged). Source data are available for this figure: SourceData F5.