Despite decades of reliance on rodent models in neuroinflammation and neurodegeneration, there is growing consensus that animal systems often fail to capture key human disease mechanisms. This panel will debate whether we are entering a postanimal-model era or simply shifting expectations and redefining how in vivo studies are used.

• What have we truly learned from animal models and where have they fallen short in reflecting the complexity of human neuroimmune diseases?
• How do chimeric and humanized mouse models help bridge the translational gap, and what are their limitations?
• When is reliance on animal models necessary, and when can strong human genetic or phenotypic data support a “modellight” approach?
• How should we balance phenotypic versus target-driven strategies in preclinical testing, especially given the artificial nature of many models (e.g., amyloid beta overexpression)?
• Are current in vitro models a step backward or an important complement in understanding multifactorial diseases where secondary mechanisms matter?
• How do different companies weigh model necessity depending on target confidence and therapeutic strategy, and what does the future hold for smarter, more selective use of in vivo models?