4.7 Article

Long-term Neural Embedding of Childhood Adversity in a Population-Representative Birth Cohort Followed for 5 Decades

期刊

BIOLOGICAL PSYCHIATRY
卷 90, 期 3, 页码 182-193

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ELSEVIER SCIENCE INC
DOI: 10.1016/j.biopsych.2021.02.971

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资金

  1. National Institute on Aging [R01AG032282, R01AG049789, T32-AG000029]
  2. Medical Research Council [MR/P005918/1]
  3. Jacobs Foundation
  4. National Institute of Environmental Health Sciences [F31ES029358]
  5. National Science Foundation Graduate Research Fellowship [NSF DGE1644868]
  6. New Zealand Health Research Council
  7. New Zealand Ministry of Business, Innovation, and Employment

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Childhood adversity is associated with widespread differences in midlife gray matter across cortical and subcortical structures, with prospectively ascertained adversity having stronger and more extensive associations than retrospectively reported adversity. These effects are distributed broadly along a hierarchical cortical gradient of information processing, indicating long-lasting biological embedding of childhood adversity in the brain.
BACKGROUND: Childhood adversity has been previously associated with alterations in brain structure, but heterogeneous designs, methods, and measures have contributed to mixed results and have impeded progress in mapping the biological embedding of childhood adversity. We sought to identify long-term differences in structural brain integrity associated with childhood adversity. METHODS: Multiple regression was used to test associations between prospectively ascertained adversity during childhood and adversity retrospectively reported in adulthood with structural magnetic resonance imaging measures of midlife global and regional cortical thickness, cortical surface area, and subcortical gray matter volume in 861 (425 female) members of the Dunedin Study, a longitudinal investigation of a population-representative birth cohort. RESULTS: Both prospectively ascertained childhood adversity and retrospectively reported adversity were associated with alterations in midlife structural brain integrity, but associations with prospectively ascertained childhood adversity were consistently stronger and more widely distributed than associations with retrospectively reported childhood adversity. Sensitivity analyses revealed that these associations were not driven by any particular adversity or category of adversity (i.e., threat or deprivation) or by childhood socioeconomic disadvantage. Network enrichment analyses revealed that these associations were not localized but were broadly distributed along a hierarchical cortical gradient of information processing. CONCLUSIONS: Exposure to childhood adversity broadly is associated with widespread differences in midlife gray matter across cortical and subcortical structures, suggesting that biological embedding of childhood adversity in the brain is long lasting, but not localized. Research using retrospectively reported adversity likely underestimates the magnitude of these associations. These findings may inform future research investigating mechanisms through which adversity becomes embedded in the brain and influences mental health and cognition.

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