Gene expression networks in rTg4510 mice generated by IPA appeared very similar to those identified in AD, with complement pathways representing a major subnetwork centered around a hub formed by the gene, Tyrobp. While complement activation is a well-described pathological feature of AD, the role of complement in neurodegenerative disease has received renewed interest as genome-wide association studies (GWAS) have identified alleles of the gene encoding complement component (C3b/C4b) receptor 1, CR1, as conferring substantial risk for AD [18], [40]–[44]. This evidence concerns the gene TYROBP and neurodegenerative disease.