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Early adversity (EA) has been shown to be a potent risk factor for developing a psychopathology in adulthood. Alterations of the stress system in addition to changes in brain development have been suggested to explain some of the psychopathologies associated with EA. The stress response involves the activation of the hypothalamic-pituitary-adrenal (HPA)-axis, which leads to the production of glucocorticoids (GCs; cortisol in humans). Being soluble in lipids, GCs easily cross the blood brain barrier and access GC receptors in the hippocampus, prefrontal cortex and amygdala. These three brain structures do not develop at the same rhythm in humans and recent models suggest that exposition to EA at different times throughout cerebral development can induce a differential vulnerability to diverse mental illnesses. Although these models are of interest, they do not provide any mechanism(s) through which exposition to EA could lead to an increased vulnerability to certain mental illnesses and not others. Interestingly, the main brain structures that are affected by the chronic secretion of stress hormones during childhood (hippocampus, prefrontal cortex and amygdala) are differentially involved in various cognitive functions (memory, emotion regulation, encoding of emotional memories, etc.). It is therefore proposed that exposure to EA, by affecting the development of specific brain structures, might alter the underlying cognitive process of these brain regions, and increase vulnerability to specific mental disorders in adulthood.Early adversity (EA) is a risk factor developing psychopathologies in adulthood.The stress system is altered in children and adults who undergone EA.EA is linked with altered brain structures and activations involved in cognition.Integrating stress, brain, and cognition, in a comprehensive model might be key.Such comprehensive model might inform the risk to develop EA-related pathologies.