Elucidating the Role of CLEC7A in Tau-Mediated Neurodegenerative Disease


Great strides have been made recently in defining how the professional immune and waste disposal cells of the brain (i.e., microglia) change during the course of Alzheimer’s disease (AD) progression. From these studies, CLEC7A routinely has been identified as one of the molecules most highly upregulated by microglia in various AD models. While CLEC7A has emerged as a commonly used marker of microglial activation in Alzheimer’s disease, little is known currently in regard to its roles in microglial biology and neurodegenerative disease. In this proposal, we will bridge this gap in knowledge through studies that will define how genetic ablation of CLEC7A influences microglial responses, neuroinflammation, brain pathology and cognitive function in a tau-mediated model of Alzheimer’s disease. To gain insights into the therapeutic potential of targeting CLEC7A to treat tauopathy, we also will interrogate how pharmacological modulation of CLEC7A activation impacts tau-driven neurodegenerative disease progression. Completion of these studies will break new ground in our understanding of the innate immune pathways that impact neurodegenerative disease pathogenesis, and also will help to establish a new molecular player (i.e., CLEC7A) that can be targeted to treat Alzheimer’s disease.

Funding to Date



Studies of Innate Immune Pathology, Translational


John R. Lukens, Ph.D.