In this review, we report on studies that have assessed the effects of exogenous and endogenous increases in stress hormones on human cognitive performance. We first describe the history of the studies on the effects of using exogenous stress hormones such as glucocorticoids as anti-inflammatory medications on human cognition and mental health. Here, we summarize the cases that led to the diagnosis of glucocorticoid-induced 'steroid psychosis' in human populations and which demonstrated that these stress hormones could thus cross the blood-brain barrier and access the brain where they could influence cognition and mental health. We then summarize studies that assessed the effects of the exogenous administration of glucocorticoids on cognitive performance supported by the hippocampus, the frontal lobes and amygdala. In the second section of the paper, we summarize the effects of the endogenous release of glucocorticoids induced by exposure to a stressful situation on human cognition and we further dissociate the effects of emotion from those of stress on human learning and memory. Finally, in the last section of the paper, we discuss the potential impact that the environmental context to which we expose participants when assessing their memory could have on their reactivity to stress and subsequent cognitive performance. In order to make our point, we discuss the field of memory and aging and we suggest that some of the 'age-related memory impairments' observed in the literature could be partly due to increased stress reactivity in older adults to the environmental context of testing. We also discuss the inverse negative correlations reported between hippocampal volume and memory for young and older adults and suggest that these inverse correlations could be partly due to the effects of contextual stress in young and older adults, as a function of age-related differences in hippocampal volume.

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Early-life stress (ES) has been associated with diverse forms of psychopathology. Some investigators suggest that these associations reflect the effects of stress on the neural circuits that support cognitive control. However, very few prior studies have examined the associations between ES, cognitive control, and underlying neural architecture. The present study compares adolescents with a documented history of ES to typical adolescents on a cognitive control task using functional magnetic resonance imaging (fMRI). Twelve ES adolescents who were adopted because of early caregiver deprivation (9 females, age = 13 years ± 2.58) and 21 healthy control adolescents without a history of ES (10 females, age = 13 years ± 1.96) who resided with their biological parents performed the change task (Nelson et al., 2007) -a variant of the stop taskduring fMRI. Behaviourally, ES adolescents took longer to switch from a prepotent response ("go") to an alternative response ("change") than control adolescents. During correct "change" responses vs. correct "go" responses, this behavioural group difference was accompanied by higher activation in ES subjects than controls. These differences were noted in regions involved in primary sensorimotor processes (pre-and postcentral gyri), conflict monitoring (dorsal anterior cingulate gyrus), inhibitory and response control (inferior prefrontal cortex and striatum), and somatic representations (posterior insula). Furthermore, correct "change" responses vs. incorrect "change" responses recruited the inferior prefrontal cortex (BA 44/46) more strongly in ES subjects than controls. These data suggest impaired cognitive control in youth who experienced ES.