It has been proposed that systemic inflammation in the pathogenesis of Alzheimer’s disease (AD) is primarily considered a contributor to the disease process. Communication between the central and peripheral immune systems may also be necessary for AD. Increased infiltration of monocytes and other adaptive immune cells into the brain has been reported with ageing and seen in AD mouse models and human AD brains. The infiltrating cells' responses can substantially impact the neuroinflammatory environment and AD pathology progression. However, the consequences are complex, whether detrimental or beneficial. The role of infiltrated monocytes appears to be influenced by a number of factors. Using single-cell genomics will help us elucidate the characteristics of infiltrated monocytes and cross-talk between peripheral and central nervous systems. We want to investigate different subsets of monocytes from bone marrow and microglia from the brain and how systemic inflammation affects pathology in CNS before and after plaque deposition.