Abstract Alzheimer’s disease (AD) is a progressive inflammatory neurodegenerative disorder leading to debilitating cognitive dysfunction, and is still without cure or effective prevention options. Several studies demonstrated that low grade inflammation in the brain is associated with higher risk of AD. Patients with AD exhibit an overproduction of the pro-inflammatory cytokine interleukin-1 beta (IL-1β) in the cerebrospinal fluid and brain tissue. Importantly, exaggerated IL-1β levels robustly inhibit synaptic plasticity mechanisms critical for normal memory function. In this application we will determine the function of members of the canonical and non- canonical inflammasome in relation of AD.