At a joint Keystone symposia, microglia continued to twist and turn in the limelight, casting a long shadow as central agents of disease, not mere responders. Researchers embraced the complex reality of mixed pathology, dishing out data from animal models in which Aβ, tau, and α-synuclein mingled and sparked each other’s spread. From a gut-initiated model of Parkinson’s disease to chimeric mice harboring human microglia to a startling conversion of astrocytes to newborn dopaminergic neurons within the brain, researchers upped the ante on disease models and proposed new therapeutic strategies.