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Published on: December 2, 2015
Ancestral, Pregnancy, and Negative Early-Life Risks Shape Children's Brain (Dis)similarity to Schizophrenia
Peter Kochunov1, Yizhou Ma1, Kathryn S Hatch1
1Maryland Psychiatric Research Center, Department of Psychiatry, University of Maryland School of Medicine, Baltimore, Maryland.
Insights
Familial and environmental risks for schizophrenia spectrum disorder (SSD) can alter brain development in children, creating patterns similar to adult SSD patients before symptoms appear. This suggests early brain changes may indicate future risk.
Area of Science:
- Neuroscience
- Developmental Psychology
- Psychiatry
Background:
- Schizophrenia spectrum disorder (SSD) is linked to familial, obstetric, and early-life environmental risks that disrupt normal brain development.
- These risks may lead to brain deficit patterns resembling those in adult SSD patients, even before symptom onset in children.
Approach:
- Utilized data from the Adolescent Brain Cognitive Development (ABCD) Study (N=8940) including children with a family history of SSD (N=727).
- Employed a regional vulnerability index to assess alignment of children's brain patterns with adult SSD deficit patterns.
- Evaluated effects of ancestral SSD history, pre/perinatal environment, and early-life experiences on brain development.
Key Points:
- The regional vulnerability index captured more variance in ancestral SSD history compared to traditional brain measurements in children with a family history of SSD.
- This index also better explained variance related to negative pre/perinatal and early-life environments in children, regardless of family history.
- Findings indicate that genetic and environmental risks can subtly alter brain patterns in children, mirroring those seen in adult SSD.
Conclusions:
- Familial, pre/perinatal, and early developmental risks can shift brain patterns in children towards those observed in adult schizophrenia spectrum disorder.
- Individual similarity to adult SSD brain patterns may serve as an early biomarker for the impact of genetic and developmental risks.
- These alterations occur prior to the emergence of psychotic or prodromal symptoms, highlighting potential for early identification.
Background:
Familial, obstetric, and early-life environmental risks for schizophrenia spectrum disorder (SSD) alter normal cerebral development, leading to the formation of characteristic brain deficit patterns prior to onset of symptoms. We hypothesized that the insidious effects of these risks may increase brain similarity to adult SSD deficit patterns in prepubescent children.
Methods:
We used data collected by the Adolescent Brain Cognitive Development (ABCD) Study (N = 8940, age = 9.9 ± 0.1 years, 4307/4633 female/male), including 727 (age = 9.9 ± 0.1 years, 351/376 female/male) children with family history of SSD, to evaluate unfavorable cerebral effects of ancestral SSD history, pre/perinatal environment, and negative early-life environment. We used a regional vulnerability index to measure the alignment of a child's cerebral patterns with the adult SSD pattern derived from a large meta-analysis of case-control differences.
Results:
In children with a family history of SSD, the regional vulnerability index captured significantly more variance in ancestral history than traditional whole-brain and regional brain measurements. In children with and without family history of SSD, the regional vulnerability index also captured more variance associated with negative pre/perinatal environment and early-life experiences than traditional brain measurements.
Conclusions:
In summary, in a cohort in which most children will not develop SSD, familial, pre/perinatal, and early developmental risks can alter brain patterns in the direction observed in adult patients with SSD. Individual similarity to adult SSD patterns may provide an early biomarker of the effects of genetic and developmental risks on the brain prior to psychotic or prodromal symptom onset.
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