Psychosis has traditionally been treated as a psychiatric disorder distinct from neurodegeneration, but new findings are challenging that boundary. From the autoimmune encephalitis spectrum to late-stage Alzheimer’s, psychotic episodes increasingly appear to be tightly linked to microglial activation, cytokine expression, and autoantibody activity. This workshop will explore the emerging hypothesis that inflammation is not just correlated with psychosis, it may be a primary driver, with IL-6 expression and glial dysfunction serving as critical mechanistic nodes. As the lines blur between psychiatric and neurological conditions, this session will unpack what that means for therapeutic development, biomarkers, and trial design.

Key Topics to Be Explored:

• Explore how psychosis manifests in Alzheimer’s, autoimmune encephalitis, and anti-NMDA receptor syndromes, pointing toward shared inflammatory underpinnings.
• Review evidence showing elevated IL-6 expression in glial cells as a predictor of psychosis in neurodegenerative disease and how existing antipsychotics may work by modulating immune pathways.
• Examine whether the location and timing of neuroinflammation, not the inflammatory trigger itself, determines whether a patient develops psychosis, depression, or cognitive decline.
• Investigate how circulating autoantibodies in psychiatric patients may represent a broader autoimmune involvement in conditions like schizophrenia and bipolar disorder.
• Discuss how inflammation-first models might inform the next generation of psychosis treatments, particularly large molecules and immune-modulating approaches.