Patrick Kesslak

Animal models remain the crucial, but often weakest, link between discovery and clinic. This workshop dissects why toxin‑based and first‑gen transgenic models miss human disease complexity and progression and showcases next‑generation options such as hybrid humanized strains, gut‑origin paradigms, and vector‑delivered pathology that better mirror biomarker change and clinical progression. Walk away with clear criteria and partnership tips for selecting, benchmarking, and refining in‑vivo systems that sharpen translational signals and cut downstream risk.

Key Questions to Be Addressed:

• What criteria should define a ‘fit-for-purpose’ in vivo model in neurodegenerative disease, especially when pathological complexity and slow disease progression challenge current paradigms?
• How can we enhance the translatability of in vivo findings to clinical endpoints, particularly in tracking neuroinflammatory, synaptic, or resilience-related pathways beyond amyloid and α-synuclein?
• With combinatorial and multi-target strategies becoming more common, how do we best model additive or synergistic effects across amyloid, tau, α-synuclein, and neuroinflammatory cascades?
• What role can newer disease paradigms, such as gut-brain axis induction or viral vector delivery, play in enhancing the physiological relevance of current models?
• How do we benchmark CROs and academic centres developing novel models? What best practices and vendor collaborations can accelerate model refinement and validation?