Explore the Agenda

8:00 am Check In, Coffee & Light Breakfast

Target Discovery Track

9:00 am Workshop A: Neuroinflammation & Neuroimmune Pathways as a Common Thread in Early-Onset & Neurodegenerative Psychosis

Senior Group Leader, Broad Institute of MIT & Harvard
President & Chief Executive Officer, Arialys Therapeutics

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.

Translational Tools Track

9:00 am Workshop B: Advancing Biomarker Discovery in Neuroinflammatory Disease

Research Director, Division of Neuroimmunology & Neuroinfectious Disease, Massachusetts General Hospital

Advances in molecular and cellular technologies have expanded the toolkit for biomarker discovery, yet distinguishing meaningful signals from background noise remains a central challenge. Fluid based, cellular and tissue level analyses offer new insight into disease biology, but their translational value hinges on careful validation and clear links to underlying mechanisms. This workshop will examine current strategies for identifying and validating biomarkers in neuroimmunology, the limitations of relying solely on RNA or protein based readouts, the role of patient samples, biobanks and computational approaches, and how the field is moving toward greater clinical relevance and impact.

Key Topics to Be Explored:

  • Review strategies for identifying novel biomarkers in neuroinflammatory and neurodegenerative diseases using molecular, cellular, and fluid-based approaches
  • Evaluate how potential biomarkers are validated experimentally, and the importance of functional studies in linking biomarker candidates to disease mechanisms
  • Examine the limitations of RNA or protein-based biomarkers and the challenges of correlating molecular signals with disease outcomes
  • Discuss the role of patient samples, biobanks and machine learning in advancing biomarker discovery
  • Highlight current gaps in biomarker development and strategies to increase translational relevance and clinical applicability

12:00 pm Lunch Break & Networking

Target Discovery Track

1:00 pm Workshop C: The Role of Inflammation in the Biology of Mood Disorders

Principal Scientist, IGC PHARMA

Neuropsychiatric symptoms have long been approached from a behavioural lens, often leading to treatments that address symptoms without a clear mechanistic understanding of their root causes. However, recent advances in neuroimmunology are reframing mood disorders, especially late-onset and comorbid depression, as potentially biologically driven diseases with immune system involvement. This workshop will tackle the growing body of evidence suggesting that chronicinflammation, glial dysfunction, and even systemic immune activation play a key role in the onset and progression of depressive disorders. Through cross-disciplinary discussion, we’ll ask whether psychiatry is ready for a shift toward biologically targeted therapeutics and what that would require in terms of biomarkers, models, and trial strategy.

Key Topics to Be Explored:

  • Examine the bidirectional relationship between immune activation and mood disorders – is neuroinflammation causative, or does it amplify pre-existing vulnerabilities?
  • Discuss how shared inflammatory mechanisms in neurodegenerative diseases (e.g., Parkinson’s, Alzheimer’s) are helping redefine depression as a neurobiological condition rather than a purely psychological one
  • Explore how lifestyle factors such as stress and substance use may initiate or exacerbate neuroinflammatory cascades contributing to depressive symptoms
  • Evaluate emerging therapeutic approaches, including small and large molecules, aimed at modulating the immune system as a treatment for depression
  • Highlight the critical need for robust biomarkers that can stratify patients based on inflammatory profiles and reduce placebo effects in depression trials

Translational Tools Track

1:00 pm Workshop D: Preclinical Strategy: In Vitro Models for Neuroimmunology: Accelerating Proof of Concept Without In Vivo Dependencies

Scientific Executive Director, Bristol Myers Squibb
Associate Director - Target Discovery & Genomics, Alector

As neuroimmunology drug development pushes toward greater translational efficiency, in vitro systems, especially patient-derived and cell-based models are gaining traction as alternatives to traditional animal studies. This workshop will examine how in vitro data can be used more strategically to justify clinical entry, where current models fall short, and how evolving regulatory perspectives are reshaping preclinical expectations.

Key Topics to Be Explored:

  • Can cell-based efficacy data replace animal models as a viable route to early proof of concept in neuroimmune drug development?
  • How can in vitro systems be optimized to model specific features or symptoms of complex CNS disorders, rather than entire disease pathologies?
  • What role do patient-derived cells, co-culture systems, and human-relevant endpoints play in bridging preclinical and clinical evidence?
  • How are regulatory agencies interpreting mechanistic in vitro data in the absence of strong in vivo correlation or validated biomarkers?
  • When does strong human genetic evidence outweigh the need for extensive model validation and how can earlystage companies tailor their strategy accordingly?
  • What lessons can be drawn from recent FDA or EMA submissions where in vitro results played a central role in moving programs forward?

4:00 pm End of Pre-Conference Workshop Day