the potential causality of this pathway in LOAD pathology. In fact, the dissection of the immune/microglia module into distinct families and key causal regulators point towards an important function of the microglia pathways involving genes of the ‘Complement’ and/or ‘Fc’ network clusters. Figure S5 (genes marked in red) highlight many of the key genes in the pathogen phagocytosis pathways found in the immune/microglia module. It is noteable how comprehensive representation of a specific signal transduction pathways is observed within the two immune families of this module. The strategic network position of TYROBP as a causal regulator of many genes mirrors its bottleneck position in several microglia activation signaling cascades. Extrapolating from this data-driven interaction, it is possible that TYROBP may be associated with neuronal pruning activity of the complement system that may be reawakened in LOAD via amyloid-β and Tau aggregates (Stevens, 2007; Perry, 2010). In this manner, the network structure can become a data-driven hypothesis generator for novel disease-relevant interactions.
