With the general notion that innate immune responses in the brain, including those related to neuronal stress, act to some extent to favor recovery, we sought to determine if the inflammatory responses to neuronal stress—especially IL-1β—positively influence mechanisms known to be necessary for autophagic clearance of unwanted proteins and cellular entities that characterize AD and other neurodegenerative diseases. This evidence concerns the gene IL1B and neurodegenerative disease.