Schizophrenia research · 2025
Altered brain activation during memory retrieval mediates the relationship between developmental trauma and psychotic symptom severity.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Mason Ava J C, Palmer William, Cao Hengyi, Addington Jean, Bearden Carrie E, Cadenhead Kristin S, Cornblatt Barbara A, Perkins Diana O, Mathalon Daniel H, Walker Elaine F, Woods Scott W, Cannon Tyrone D
Аннотация
BACKGROUND: Developmental trauma (DT) and poorer episodic memory performance are associated with increased risk of psychotic symptoms, but the mechanisms underlying these associations remain to be established. We sought to investigate whether memory performance and fMRI activity during the retrieval phase of an associative episodic memory task statistically mediated the relationship between trauma multiplicity and psychotic symptom severity in youth at clinical high risk for psychosis.
METHODS: Measures from 795 participants in the North American Prodrome Longitudinal Study (phase two) were analysed. This included the Childhood Trauma and Abuse scale, neurocognitive measures, the Scale of Psychosis-Risk Symptoms and, in a subsample, neural activation from five regions of interest associated with memory processing (n = 219) during a paired-associate memory task (data from this task; n = 198). Linear regressions were conducted to measure whether trauma multiplicity predicted subclinical delusion and hallucination severity and neurocognitive performance, and neurocognitive measures predicted subclinical hallucination or delusion severity. We used mediation analysis when all paths were significant.
RESULTS: Average functional activation in the five memory-associated regions mediated 8.74 % of the association between DT and subclinical hallucination severity, and 7.02 % between DT and delusion severity. Inferior parietal lobe activity mediated 10.08 % of the association between DT and subclinical hallucination severity, and 8.7 % between DT and subclinical delusion severity.
CONCLUSIONS: These findings suggest a role of episodic memory processing and inferior parietal lobe activation in the association between DT and psychosis. Focusing further on these measures could provide insight into the underlying mechanism of this association, and have clinical implications in trauma-exposed individuals with psychosis.
METHODS: Measures from 795 participants in the North American Prodrome Longitudinal Study (phase two) were analysed. This included the Childhood Trauma and Abuse scale, neurocognitive measures, the Scale of Psychosis-Risk Symptoms and, in a subsample, neural activation from five regions of interest associated with memory processing (n = 219) during a paired-associate memory task (data from this task; n = 198). Linear regressions were conducted to measure whether trauma multiplicity predicted subclinical delusion and hallucination severity and neurocognitive performance, and neurocognitive measures predicted subclinical hallucination or delusion severity. We used mediation analysis when all paths were significant.
RESULTS: Average functional activation in the five memory-associated regions mediated 8.74 % of the association between DT and subclinical hallucination severity, and 7.02 % between DT and delusion severity. Inferior parietal lobe activity mediated 10.08 % of the association between DT and subclinical hallucination severity, and 8.7 % between DT and subclinical delusion severity.
CONCLUSIONS: These findings suggest a role of episodic memory processing and inferior parietal lobe activation in the association between DT and psychosis. Focusing further on these measures could provide insight into the underlying mechanism of this association, and have clinical implications in trauma-exposed individuals with psychosis.