Neuroimmune Consortium: Effects of Peripheral Inflammation on Myeloid Cell Function in Alzheimer’s Disease


Increasing evidence from our lab and others indicates that immune cells in the central nervous system (CNS) exist in diverse homeostatic states that are rapidly disrupted by inflammation and signals from the periphery. Alzheimer’s disease (AD) is marked by neuroinflammatory dysfunction, but it is unclear how this dysfunction interacts with AD pathology. This proposal aims to leverage human and mouse models of AD to investigate how inflammatory signals from the body alter the neuroimmune landscape of the brain and how this, in turn, affects AD pathology and cognitive dysfunction. Understanding how inflammatory signals from across the body are communicated to the brain may be a key component of understanding how to slow the onset and progression of AD.

Funding to Date



Studies of Innate Immune Pathology, Translational


Beth Stevens, Ph.D.