New drugs often fail in the translation from the rodent experimental autoimmune encephalomyelitis (EAE) model to human multiple sclerosis (MS). Here, we present the marmoset EAE model as an indispensable model for translational research into MS. The genetic heterogeneity of this species and lifelong exposure to chronic latent infections and environmental pathogens create a human-like immune system. Unique to this model is the presence of the pathological hallmark of progressive MS, in particular cortical grey matter lesions. Another great possibility of this model is systemic and longitudinal immune profiling, whereas in humans and mice immune profiling is usually performed in a single compartment (i.e. blood or spleen, respectively). Overall, the marmoset model provides unique opportunities for systemic drug-effect profiling.
Rodent models have their problems but they and the human dimensions need to be addressed.
Baker D, Amor S. Mouse models of multiple sclerosis: lost in translation? Curr Pharm Des. 2015;21:2440-52
Baker D, Amor S Experimental autoimmune encephalomyelitis is a good model of multiple sclerosis if used wisely 3, p555–564
Likewise, we can ask where primates have been more successful over their rodent counterparts? The literature is full of marmoset studies on treatments that have gone nowhere. Is that the fault of the idea, model or the clinical trial.
The disastrous “elephant head” anti-CD28 super agonist trial that made people loose their toes and fingers was tested in marmosets.
The speed at which animals accumulate damage depends on which strain you use and how you induce the disease.
Why do we use non-human primates studies….as a safety tool before going into humans or as a research tool to find treatments? But can you ever do experiments in enough marmosets to be confident?
What are your thoughts