For decades, researchers have targeted amyloid and tau proteins in their efforts to understand Alzheimer’s disease and develop therapeutics to combat it, but focusing on amyloid and tau has not yielded therapeutics that dramatically impact the course of disease. An established and growing body of literature supports a link between neuroinflammation and Alzheimer’s pathology, suggesting powerful new therapeutic approaches.

MindImmune’s R&D has explored and understood the inflammatory drivers of degenerative CNS disorders like Alzheimer’s, uncovering that CD11c+ cells, a subset of innate immune cells originating in the periphery can be recruited into the brain where they surround amyloid plaques. In the brain, these cells play a key role in Alzheimer’s disease pathogenicity by driving neuro-inflammatory processes that result in the destruction of the synapses essential to healthy neural connections, resulting both in the cognitive symptoms and relentless progression of Alzheimer’s disease. We have generated preclinical data in mouse models of Alzheimer’s disease demonstrating that eliminating CD11c+ cells reduces signs of synaptic dystrophy.

MindImmune is developing a therapeutic monoclonal antibody (MITI-101) designed to block recruitment of CD11c+ innate immune cells into the brain, which will prevent the cells from causing the synaptic damage that drives cognitive symptoms and progression in Alzheimer’s disease.

Blocking these immune cells from entering the brain prevents the damage they do to synapses.  Synaptic damage is the core pathology in Alzheimer’s disease, causing the day-to-day cognitive symptoms as well as the insidious progression of the disease. Thus, blocking immune cell recruitment may improve cognitive symptoms and slow the progression of this devastating disease.