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The Effect of Developmental Trauma on Brain Structures Involved in Threat and Memory Processing and Its Relation to Psychotic Experiences in Adulthood
The Effect of Developmental Trauma on Brain Structures Involved in Threat and Memory Processing and Its Relation to Psychotic Experiences in Adulthood
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The Effect of Developmental Trauma on Brain Structures Involved in Threat and Memory Processing and Its Relation to Psychotic Experiences in Adulthood
The Effect of Developmental Trauma on Brain Structures Involved in Threat and Memory Processing and Its Relation to Psychotic Experiences in Adulthood

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The Effect of Developmental Trauma on Brain Structures Involved in Threat and Memory Processing and Its Relation to Psychotic Experiences in Adulthood
The Effect of Developmental Trauma on Brain Structures Involved in Threat and Memory Processing and Its Relation to Psychotic Experiences in Adulthood
Journal Article

The Effect of Developmental Trauma on Brain Structures Involved in Threat and Memory Processing and Its Relation to Psychotic Experiences in Adulthood

2025
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Overview
Despite growing evidence of a causal association between developmental trauma (DT) and psychotic experiences (PEs), the precise neurobiological mechanisms underlying this association remain poorly understood. We examined the effect of DT on the structure of brain regions involved in threat and memory processing, and the role of these alterations in the association between DT and PEs. This study used data from the Avon Longitudinal Study of Parents and Children, a large, population-based birth cohort in the United Kingdom. Data were available from 419 participants, including DT reported by the parents or the participants between ages 0 and 17 years, PEs at age 18, and volumes of regions involved in threat and memory processing in adulthood (mean = 21,2, SD = 1.5 years). DT exposure was associated with increased odds of PEs (odds ratio [OR] = 1.64; 95% CI, 1.04-2.59, P = .035), with evidence supporting cumulative risk effects for exposure to multiple trauma types (B = 0.160, P < .001). DT was also associated with reduced left amygdala volumes (B = -0.011, P = .02) with evidence again supporting cumulative risk effect with multiple trauma types (B = -0.006, P = .01). Reduced bilateral amygdala volume was associated with an increased odds of PEs driven by the left amygdala (OR = 0.001, 95% CI, 0.000-0.154, P = .006). These findings are consistent with theories that alterations in brain regions involved in threat and memory processing lie on the neurobiological pathway from DT to PEs, offering the possibility of prevention strategies for psychosis.

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