The marmoset monkey: a multi-purpose preclinical and translational model of human biology and disease

Abstract

The development of biologic molecules (monoclonal antibodies, cytokines, soluble receptors) as specific therapeutics for human disease creates a need for animal models in which safety and efficacy can be tested. Models in lower animal species are precluded when the reagents fail to recognize their targets, which is often the case in rats and mice. In this Feature article we will highlight the common marmoset, a small-bodied nonhuman primate (NHP), as a useful model in biomedical and preclinical translational research.

Induction of heat shock proteins in differentiated human neuronal cells following co-application of celastrol and arimoclomol

“…The present problem of therapeutic compounds, identified in rodent models of disease, that fail to translate to effective treatments in the human clinical setting could be addressed by the generation of primate animal models using the common marmoset (Lang 2010;t Hart et al 2012;McGonigle and Ruggeri 2014;Sasaki 2015). Rodent models fail to encompass the complexity of the human brain (Lang 2010;t Hart et al 2012;McGonigle and Ruggeri 2014;Sasaki 2015). Interestingly, the HSPA6 gene is found in the marmoset genome (NCBI gene ID: 100411854).…”

“…Recently, we have demonstrated a unique feature of HSPA6, namely localization to transcription sites in human neuronal cells during recovery from stress-induced inhibition (Khalouei et al 2014), a feature that is missing in current animal models of neurodegenerative diseases which lack HSPA6. The present problem of therapeutic compounds, identified in rodent models of disease, that fail to translate to effective treatments in the human clinical setting could be addressed by the generation of primate animal models using the common marmoset (Lang 2010;t Hart et al 2012;McGonigle and Ruggeri 2014;Sasaki 2015). Rodent models fail to encompass the complexity of the human brain (Lang 2010;t Hart et al 2012;McGonigle and Ruggeri 2014;Sasaki 2015).…”

“…Despite numerous clinical trials, few effective therapies for neurodegenerative diseases have been identified (Dunkel et al 2012;Pratt et al 2015). This may be due to deficiencies in current animal models to encompass the complexity of the human brain (Lang 2010;t Hart et al 2012;McGonigle and Ruggeri 2014;Sasaki 2015). Furthermore, the progression of neurodegenerative diseases is multifactorial; hence, targeted inhibition of a single disease pathology is compensated by concurrent deleterious pathways (Cavalli et al 2008;Lang 2010;Dunkel et al 2012;Huang and Mucke 2012;Sheikh et al 2013).…”

Coevolution of insulin-like growth factors, insulin and their receptors and binding proteins in New World Monkeys

“…It seems likely therefore that coevolution of these structurally-and functionally-related molecules occurred, associated with a change in their roles in regulating cellular metabolism and growth. Further information about the functions of insulin and IGFs in NWM is needed in order to be able to assess the physiological significance of this change, and such assessment seems desirable in view of the importance of NWM, especially the marmoset, as a model for human biology and disease [62].…”

Neuroscience Research Using Non-human Primate Models and Genome Editing

“…Marmoset endocrinology and metabolism are more similar to those of humans than of rodents, which is important in pharmacological and toxicological studies of new drug candidates. The marmoset is also more closely phylogenetically related to humans (Kitamura et al 2011;t'Hart et al 2003t'Hart et al , 2012. In Europe, the marmoset is now being used as a non-rodent second species in drug safety tests (Smith et al 2001).…”