Historically, reactive astrocytes and neuroinflammation were thought to arise secondary to neuronal cell death in neurodegenerative diseases with little relevance. However, astrocytes and neuroinflammation are beginning to emerge as critical components of neurological disorders that were once thought to selectively afflict neurons. Our goal is to understand the molecular mechanisms that regulate reactive astrocytes and their neurotoxicity in neurodegenerative diseases, including Alzheimer’s disease, by utilizing a combination of biochemistry, molecular biology, cellular models of inflammation and mouse models of neurodegenerative diseases. We are also interested in developing novel therapies targeting these pathways to reduce neuroinflammation for potential therapeutic intervention.