ArticleBrain imaging and behavior2015
ERBB4 polymorphism and family history of psychiatric disorders on age-related cortical changes in healthy children.
Article in Brain imaging and behavior, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.
- Genetic Influences on the Developing Young Brain and Risk for Neuropsychiatric Disorders.Biological psychiatry · 2023Pooled it
- Convex approaches to isolate the shared and distinct genetic components of complex traits.Bioinformatics (Oxford, England) · 2026Article
- Transcriptomic pathology of neocortical microcircuit cell types across psychiatric disorders.Molecular psychiatry · 2025Article
- ErbB4 precludes the occurrence of PTSD-like fear responses by supporting the bimodal activity of the central amygdala.Experimental & molecular medicine · 2024Article
- Assessment of genetic factor and depression interactions for asthma symptom severity in cohorts of childhood and elderly asthmatics.Experimental & molecular medicine · 2018Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Genetic variations in ERBB4 were associated with increased susceptibility for schizophrenia (SCZ) and bipolar disorders (BPD). Structural imaging studies showed cortical abnormalities in adolescents and adults with SCZ or BPD. However, less is known about subclinical cortical changes or the influence of ERBB4 on cortical development. 971 healthy children (ages 3-20 years old; 462 girls and 509 boys) were genotyped for the ERBB4-rs7598440 variants, had structural MRI, and cognitive evaluation (NIH Toolbox ®). We investigated the effects of ERBB4 variants and family history of SCZ and/or BPD (FH) on cortical measures and cognitive performances across ages 3-20 years using a general additive model. Variations in ERBB4 and FH impact differentially the age-related cortical changes in regions often affected by SCZ and BPD. The ERBB4-TT-risk genotype children with no FH had subtle cortical changes across the age span, primarily located in the left temporal lobe and superior parietal cortex. In contrast, the TT-risk genotype children with FH had more pronounced age-related changes, mainly in the frontal lobes compared to the non-risk genotype children. Interactive effects of age, FH and ERBB4 variations were also found on episodic memory and working memory, which are often impaired in SCZ and BPD. Healthy children carrying the risk-genotype in ERBB4 and/or with FH had cortical measures resembling those reported in SCZ or BPD. These subclinical cortical variations may provide early indicators for increased risk of psychiatric disorders and improve our understanding of the effect of the NRG1-ERBB4 pathway on brain development.
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