The Society for Neuroscience’s annual conference—the premier gathering for this very “cerebral” field—generally attracts an academic crowd.

So it’s worth noting that representatives of nearly every major pharmaceutical company attended Monday’s crowded luncheon discussion about the validity of animal models of neurodegenerative diseases.  Patrick Sweeney, Managing Director of Charles River Discovery Research Services in Finland, which sponsored the event, was happily surprised to see so many drug developers in the audience.

But is it that surprising? Research into treatments for neurological disorders has never been more intense. As the first wave of Baby Boomers turns 65, the group dubbed the Alzheimer’s generation desire solutions to this and other diseases related to aging and neurodegeneration. And scientific advances—from better imaging tools to better research models—are helping preclinical researchers elucidate the multiple mechanisms that destroy or revive neurological structure and function.

Despite the title of the talk, the consensus among yesterday’s panel was that animal models have an important role to play in the study of these puzzling diseases—from Alzheimer’s to schizophrenia—that destroy the structure and function of nerve cells. But Sweeney says the field is also starting to see a paradigm shift from the days when researchers relied on a single animal model. (As we all know, those attempts have been a big source of frustration for the neuroscience field). Models are now being used as tools to study various aspects of the disease and in order to make research effective the “toolbox” should be better understood and have more content.

For instance, during her presentation yesterday, Carol Colton, a neurological professor at Duke University who studies the inflammatory and immunomudulatory aspects of AD on the brain, said there are major immune differences between rodents and humans.

Going forward, the field will likely need to employ multiple models designed to mimic different aspects or symptoms of a single disease—such as Parkinson’s or Huntington’s—to make the results more translatable. That was certainly the opinion of Genentech scientist Kimberly Scearce-Levie, who rounded out the luncheon panel with a talk about using multiple technologies and methods in the study of tau proteins abundant in the central nervous system and the NRG1 gene that has been linked to schizophrenia.

Still, as outlined above, with a larger toolbox comes the need for a greater understanding in how to use those tools appropriately, and to recognize the limitations of the models, says Sweeney. The explosion in imaging is helping propel the field, but of equal importance, says Sweeney, are histology and behavior. 

Other speakers yesterday included UCLA neurology professor Marie-Françoise Chesselet, who spoke eloquently regarding the differences (and similarities) mouse models of Huntington and Parkinson diseases, and Sue Browne, director of CNS Discovery at Teva Pharmaceuticals, who spoke forthrightly about the promises and pitfalls of translational animal models for amyotrophic lateral sclerosis and multiple sclerosis.