To identify druggable points of interaction in the TREM2 and CD33-signalling pathways to modulate microglial/macrophage function for the treatment of AD, focusing on in vitro, in vivo methodologies using comprehensive analysis tools and pathway/systems biology approaches to understand the role of these regulators of microglia function in AD.
Multiple Genome-wide Association Studies and integrated systems biology approaches have linked genes involved in modulating and executing microglia mediated inflammation to Alzheimer’s Disease (AD). However the role of microglia-mediated molecular pathways and the ultimate causative link between inflammation or microglia activity and AD is still an under-explored area of research.
Resolving the role that AD risk genes such as TREM2 and CD33 play in modulating microglial function will be a critical step for understanding the controversial role of inflammation in AD. It will also pave the way to target these genes, or associated pathways, as potential AD disease modifying treatments.