PLX233137

GSE109906: RNAseq of cortex of 6-month old APPPS1 and APPPS1;Apoe-/- mice

• Organsim mouse
• Type RNASEQ
• Target gene
• Project ARCHS4

One of the hallmarks of Alzheimers disease is the presence of extracellular diffuse and fibrillar plaques predominantly consisting of the amyloid- (A) peptide. ApoE influences the deposition of amyloid pathology through affecting the clearance and aggregation of monomeric A in the brain. In addition to influencing A metabolism, increasing evidence suggests that apoE influences microglial function in neurodegenerative diseases. Here, we characterize the impact that apoE has on amyloid pathology and the innate immune response in APPPS1E9 and APPPS1-21 transgenic mice. We report that Apoe deficiency reduced fibrillar plaque deposition consistent with previous studies. However, fibrillar plaques in Apoe-deficient mice exhibited a striking reduction in plaque compaction. Hyperspectral fluorescent imaging using luminescent conjugated oligothiophenes identified distinct A morphotypes in Apoe-deficient mice. We also observed a significant reduction in fibrillar plaque-associated microgliosis and activated microglial gene expression in Apoe-deficient mice, along with significant increases in dystrophic neurites around fibrillar plaques. Our results suggest that apoE is critical in stimulating the innate immune response to amyloid pathology. SOURCE: Jason Ulrich (ulrichjd@wustl.edu) - Washington University