In summary, Hyman emphasized the following about Alzheimer’s disease animal models:
• Some mouse models exist that are close genocopies of inherited early-onset disease and have been well received as potentially relevant models.
• Mouse models are incomplete models of the human phenotype.
• Behavioral results in mouse models are not as robust as biochemical and neuropathological readouts.
• There is a need to better match animal models to the appropriate stage of human clinical disease.
Animal models are limited in terms of how far they can be extrapolated toward the human condition. However, compared to many other types of neurologic diseases, Alzheimer’s disease research has some very promising successes that can be built upon.
ANIMAL MODELS FOR NEURODEGENERATION
Neurodegeneration research spans Parkinson’s disease, Huntington’s disease, ammyotrophic lateral sclerosis (ALS), and multiple sclerosis, for example. Robert Ferrante, professor in the departments of neurological surgery, neurology, and neurobiology at the University of Pittsburgh, noted that much of this breakout group’s discussion centered on standardization of models and whether they accurately reflect neurodegenerative diseases. Ferrante suggested that current animal models for Huntington’s disease and ALS may accurately reflect not only patho-physiological mechanisms of human disease, but also neuropathology and behavioral phenomena. For other disorders, however, it is much more difficult.
In addition to emphasizing the need for standardization of animal models of neurodegenerative diseases, participants in this breakout also discussed enforcing standards for preclinical studies in animals and raised concerns about the publication of research that cannot be replicated. It was noted by some participants that although the NIH has set standards for conducting animal research1 and papers have described these standards, widespread adoption of these recommendations has been slow (Kilkenny et al., 2010).