Alzheimer’s disease (AD) is a devastating neurological disorder characterized by memory deficits, amyloid plaques, and neuronal death. Despite decades of research, there is still no cure, and cases are expected to triple by 2050. Evidence from humans and animals models indicates that this disease is associated with alterations in both synaptic and immune signaling, but the link is not well characterized. Determining how these pathways interact may reveal fundamental mechanisms underlying AD, and may identify novel molecular targets for developing desperately needed therapeutics.

Recent work from our lab indicates that the classical major histocompatibility complex I (MHCI) immune molecules may link immune signaling to synaptic deficits in AD. Ongoing experiments aim to identify how changes in MHCI levels contribute to synaptic pathology in AD, and whether altering MHCI signaling is an effective strategy to mitigate synapse and memory loss in AD.