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How does the human mind develop over the individual’s lifetime? This is the central question of the study of cognitive development. How does the human mind work in relation to other animal minds? This is the central question of comparative psychology. Developmental comparative psychology integrates the two questions. It tries to understand how the human mind works by understanding how it came about over time, both ontogenetically (in each individual’s life history) and phylogenetically (over the course of evolution). To do so, it compares the cognitive capacities and processes of individuals across different developmental time points as well as across species. When comparing humans to other species, the main focus is usually on our closest living relatives: the other primates, in particular the nonhuman great apes, such as chimpanzees. But for many questions, other species are of great theoretical interest too. For example, when it comes to future planning or tool use, the species cognitively most similar to humans seem to be various bird species. Developmental comparative research informs us, on the one hand, about deep cognitive continuities and commonalities of human and other minds. Such commonalities can refer to homologous cognitive faculties, which share both function and evolutionary origin in the sense that they go back to the same ancestor. This is usually the case when we find shared cognitive capacities in human and nonhuman primates (such as, to take a noncognitive example, the eyes of different primate species). But commonalities can also reflect merely analog cognitive faculties, which share a function but not the same evolutionary history and the same ancestor (like the different kinds of eyes found in mammals, insects, and many other species that share a function but no common ancestor or history). Rather, these faculties have then probably emerged independently in separate evolutionary lines—in so-called convergent evolution. At the same time, developmental comparative psychology informs us about potential discontinuities between human and other animal minds. That adult human thinking is special and very different from other forms of animal cognition is obvious. But developmental comparative psychology can help us to understand how it is that our cognition turns out to be so radically different from that of nonhuman primates despite the fact that the biological and genetic differences are ultimately not large. Humans may differ radically in their cognition from other primates, and these differences may simply be a matter of brute biology. We have a certain capacity but other species do not. The story may be more complex, however. The hardwired and biological differences may initially not be that big. Rather, what is special and unique about human cognition may arise step by step over developmental time. And this may be a matter not so much of individual maturation and learning alone; instead, language and other social and cultural influences and tools may be crucial. This entry gives an introduction to the newly emerging field of developmental comparative psychology. It summarizes central empirical findings concerning commonalities and differences in humans and other species in the next two sections. The most important theoretical approaches in the field are discussed in the final section.

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Background and objectives Typicality asymmetry in generalization refers to enhanced fear generalization when trained with typical compared to atypical exemplars. Typical exemplars are highly representative of their category, whereas atypical exemplars are less representative. Individual risk factors, such as trait anxiety, attenuate this effect, due to the high level of threat ambiguity of atypical exemplars. Although recent research provided evidence for generalization of safety behavior, it is unclear whether this generalization also follows typicality asymmetry. This study examined (1) whether participants exhibited typicality asymmetry in the generalization of safety behavior and (2) whether this effect would be attenuated by individual risk factors, such as intolerance of uncertainty and trait anxiety. Methods Participants were trained with either typical (Typical group, n = 53) or atypical (Atypical group, n = 55) exemplars in a fear and avoidance conditioning procedure. Participants acquired differential conditioned fear and costly safety behavior to the threat- and safety-related exemplars. In a following Generalization Test, the degree of safety behavior to novel exemplars of the same categories was tested. Results The Atypical group showed greater differential safety behavior responses compared to the Typical group. Higher trait anxiety was associated with lower differential safety behavior generalization, driven by an increase in generalized responding to novel safety-related exemplars. Limitations: This study used hypothetical cost instead of real cost. Conclusions Training with atypical exemplars led to greater safety behavior generalization. Moreover, individuals with high trait anxiety show impaired safety behavior generalization.

Objective: Specific phobia is a common anxiety disorder, but the literature on associated brain structure alterations exhibits substantial gaps. The ENIGMA Anxiety Working Group examined brain structure differences between individuals with specific phobias and healthy control subjects as well as between the animal and blood-injection-injury (BII) subtypes of specific phobia. Additionally, the authors investigated associations of brain structure with symptom severity and age (youths vs. adults). Methods: Data sets from 31 original studies were combined to create a final sample with 1,452 participants with phobia and 2,991 healthy participants (62.7% female; ages 5–90). Imaging processing and quality control were performed using established ENIGMA protocols. Subcortical volumes as well as cortical surface area and thickness were examined in a preregistered analysis. Results: Compared with the healthy control group, the phobia group showed mostly smaller subcortical volumes, mixed surface differences, and larger cortical thickness across a substantial number of regions. The phobia subgroups also showed differences, including, as hypothesized, larger medial orbitofrontal cortex thickness in BII phobia (N=182) compared with animal phobia (N=739). All findings were driven by adult participants; no significant results were observed in children and adolescents. Conclusions: Brain alterations associated with specific phobia exceeded those of other anxiety disorders in comparable analyses in extent and effect size and were not limited to reductions in brain structure. Moreover, phenomenological differences between phobia subgroups were reflected in diverging neural underpinnings, including brain areas related to fear processing and higher cognitive processes. The findings implicate brain structure alterations in specific phobia, although subcortical alterations in particular may also relate to broader internalizing psychopathology.