From humans to model organisms: Translational insights into sociability and social dysfunction

Sociability is an evolutionarily conserved biological trait that promotes information exchange, protection, cooperation, and reproductive success. Its expression nevertheless differs substantially across species, from aggregation and social recognition to affiliation, cooperation, and higher-order social cognition. This review establishes a comparative, component-based framework for evaluating what different model organisms can and cannot reveal about human sociability and social dysfunction. We compare social-cue detection, recognition and memory, motivation and reward, contextual integration, and behavioral output across humans, non-human primates, rodents, sheep, zebrafish, frogs, Drosophila, bees, and Caenorhabditis elegans. Humans provide the reference framework, integrating conserved social processes with higher-order capacities such as empathy and Theory of Mind. Autism spectrum disorder is considered as an important translational example of how alterations across partially separable social components can produce heterogeneous phenotypes. Non-human primates permit investigation of social attention, gaze, affiliation, reciprocity, and social reward within neural systems broadly homologous to those of humans. Rodents enable genetic and circuit-level analysis of social approach, recognition, memory, bonding, and parental behavior, whereas sheep support ethologically grounded studies of individual recognition, maternal-offspring bonding, and group cohesion. Zebrafish and frogs provide complementary access to the development and sensory organization of vertebrate social behavior. Drosophila, bees, and C. elegans offer genetic precision for investigating aggregation, communication, social organization, and conserved molecular mechanisms. No single species reproduces the full complexity of human sociability or a complete clinical disorder. Instead, each provides experimental access to particular social components and mechanisms, with distinct strengths and interpretive limitations. Integrating findings across complementary models can therefore clarify the biological organization of sociability and strengthen translation to human social dysfunction.