Exposure to childhood adversity is common and a powerful risk factor for many forms of psychopathology. In this opinion piece, we argue for greater translation of knowledge about the developmental processes that are influenced by childhood adversity into targeted interventions to prevent the onset of psychopathology. Existing evidence has consistently identified several neurodevelopmental pathways that serve as mechanisms linking adversity with psychopathology. We highlight three domains in which these mechanisms are well-established and point to clear targets for intervention: 1) threat-related social information processing biases; 2) heightened emotional reactivity and difficulties with emotion regulation; and 3) disruptions in reward processing. In contrast to these established pathways, knowledge of how childhood adversity influences emotional learning mechanisms, including fear and reward learning, is remarkably limited. We see the investigation of these mechanisms as a critical next step for the field that will not only advance understanding of developmental pathways linking childhood adversity with psychopathology, but also provide clear targets for behavioral interventions. Knowledge of the mechanisms linking childhood adversity with psychopathology has advanced rapidly, and the time has come to translate that knowledge into clinical interventions to prevent the onset of mental health problems in children who have experienced adversity.

Schizophrenia is associated with subtle abnormalities in day-to-day social behaviors, including a tendency in some patients to “keep their distance” from others in physical space. The neural basis of this abnormality, and related changes in social functioning, is unknown. Here we examined, in schizophrenic patients and healthy control subjects, the functioning of a parietal–frontal network involved in monitoring the space immediately surrounding the body (“personal space”). Using fMRI, we found that one region of this network, the dorsal intraparietal sulcus (DIPS), was hyper-responsive in schizophrenic patients to face stimuli appearing to move towards the subjects, intruding into personal space. This hyper-responsivity was predicted both by the size of personal space (which was abnormally elevated in the schizophrenia group) and the severity of negative symptoms. In contrast, in a second study, the activity of two lower-level visual areas that send information to DIPS (the fusiform face area and middle temporal area) was normal in schizophrenia. Together, these findings suggest that changes in parietal–frontal networks that support the sensory-guided initiation of behavior, including actions occurring in the space surrounding the body, contribute to social dysfunction and negative symptoms in schizophrenia.

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BackgroundSubclinical delusional ideas, including persecutory beliefs, in otherwise healthy individuals are heritable symptoms associated with increased risk for psychotic illness, possibly representing an expression of one end of a continuum of psychosis severity. The identification of variation in brain function associated with these symptoms may provide insights about the neurobiology of delusions in clinical psychosis.MethodsA resting-state functional magnetic resonance imaging scan was collected from 131 young adults with a wide range of severity of subclinical delusional beliefs, including persecutory ideas. Because of evidence for a key role of the amygdala in fear and paranoia, resting-state functional connectivity of the amygdala was measured.ResultsConnectivity between the amygdala and early visual cortical areas, including striate cortex (V1), was found to be significantly greater in participants with high (n = 43) v. low (n = 44) numbers of delusional beliefs, particularly in those who showed persistence of those beliefs. Similarly, across the full sample, the number of and distress associated with delusional beliefs were positively correlated with the strength of amygdala-visual cortex connectivity. Moreover, further analyses revealed that these effects were driven by those who endorsed persecutory beliefs.ConclusionsThese findings are consistent with the hypothesis that aberrant assignments of threat to sensory stimuli may lead to the downstream development of delusional ideas. Taken together with prior findings of disrupted sensory-limbic coupling in psychosis, these results suggest that altered amygdala-visual cortex connectivity could represent a marker of psychosis-related pathophysiology across a continuum of symptom severity.