PRJNA219136
Whole brain transcriptional changes in the APPswe/PS1dE9 mouse model of Alzheimer’s disease resulting from IL-10 deficiency
While neuroinflammation is a widely accepted participant in Alzheimer''s disease pathology, the impact of inflammatory suppressor pathways are poorly understood. To determine whether deficiency in the anti-inflammatory cytokine IL-10 impacted AD-like pathology, IL-10 was genetically removed from the APP/PS1 mouse model of cerebral amyloidosis. To assess the global transcriptional changes in the brains of APP/PS1 mice deficient in IL-10, RNAseq of poly(A) enriched transcripts was performed. Total brain mRNA was isolated from 12 months old APP/PS1: IL-10+/+, IL-10+/-, IL-10-/- animals (5 per group). This analysis revealed modulation of select innate immune genes that drive AD-like neuroinflammation.