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Background: Family environment has long been known for shaping brain function and psychiatric phenotypes, especially during childhood and adolescence. Accumulating neuroimaging evidence suggests that across different psychiatric disorders, common phenotypes may share common neural bases, indicating latent brain-behavior relationships beyond diagnostic categories. However, the influence of family environment on the brain-behavior relationship from a transdiagnostic perspective remains unknown., Methods: We included a community-based sample of 699 participants (ages 5-22 years) and applied partial least squares regression analysis to determine latent brain-behavior relationships from whole-brain functional connectivity and comprehensive phenotypic measures. Comparisons were made between diagnostic and nondiagnostic groups to help interpret the latent brain-behavior relationships. A moderation model was introduced to examine the potential moderating role of family factors in the estimated brain-behavior associations., Results: Four significant latent brain-behavior pairs were identified that reflected the relationship of dissociable brain network and general behavioral problems, cognitive and language skills, externalizing problems, and social dysfunction, respectively. The group comparisons exhibited interpretable variations across different diagnostic groups. A warm family environment was found to moderate the brain-behavior relationship of core symptoms in internalizing disorders. However, in neurodevelopmental disorders, family factors were not found to moderate the brain-behavior relationship of core symptoms, but they were found to affect the brain-behavior relationship in other domains., Conclusions: Our findings leveraged a transdiagnostic analysis to investigate the moderating effects of family factors on brain-behavior associations, emphasizing the different roles that family factors play during this developmental period across distinct diagnostic groups., (Copyright © 2024 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

Background: Volumetric alterations of subcortical structures as predictors of antipsychotic treatment response have been previously corroborated, but less is known about whether their morphological covariance relates to treatment outcome and is driven by gene expression and epigenetic modifications. Methods: Subcortical volumetric covariance was analyzed by using baseline T1-weighted magnetic resonance imaging (MRI) in 38 healthy controls and 38 drug-naïve first-episode schizophrenia patients. Patients were treated with 8-week risperidone monotherapy and divided into responder and non-responder groups according to the Remission in Schizophrenia Working Group (RSWG). We utilized partial least squares (PLS) regression to examine the spatial associations between gene expression of subcortical structures from a publicly available transcriptomic dataset and between-group variances of structural covariance. The peripheral DNA methylation (DNAm) status of a gene of interest (GOI), overlapping between genes detected in the PLS and 108 schizophrenia candidate gene loci previously reported, was examined in parallel with MRI scanning. Results: In the psychotic symptom dimension, non-responders had a higher baseline structural covariance in the putamen–hippocampus–pallidum–accumbens pathway compared with responders. For disorganized symptoms, significant differences in baseline structural covariant connections were found in the putamen–hippocampus–pallidum–thalamus circuit between the two subgroups. The imaging variances related to psychotic symptom response were spatially related to the expression of genes enriched in neurobiological processes and dopaminergic pathways. The DNAm of GOI demonstrated significant associations with patients' improvement of psychotic symptoms. Conclusion: Baseline subcortical structural covariance and peripheral DNAm may relate to antipsychotic treatment response. Phenotypic variations in subcortical connectome related to psychotic symptom response may be transcriptomically and epigenetically underlaid. This study defines a roadmap for future studies investigating multimodal imaging epigenetic biomarkers for treatment response in schizophrenia. [ABSTRACT FROM AUTHOR]

Despite the fast growing interest in the impact of microbiome–gut–brain interaction on regulating emotional behavior in animals, the underlying mechanisms on how brain anatomy together with gut microbiotic condition jointly influence emotional state in healthy human volunteers remain largely unknown and hypothetic. Here, high-resolution structural magnetic resonance imaging data, stool samples, and psychological assessment results on anxiety level were collected from 61 healthy adults. Voxel-based morphometry was used to assess gray matter (GM) volumes, whereas 16s rRNA gene sequencing was used for bacterial classification. Correlation and mediation analysis were conducted to quantify the relationships among regional GM volume, gut microbiome diversity, and anxiety level. We observed that anxiety level was negatively correlated with GM volume in the right dorsolateral prefrontal cortex and alpha diversity index of gut microbiome. Additional mediation analysis revealed the indirect effect of dorsolateral prefrontal cortex GM volume on anxiety level via gut microbiome diversity. Our findings provide potential evidence of the microbiome–gut–brain interactions and their association with anxiety, highlighting gut microbiome diversity as a mediator that influences the relationship between brain morphometry and anxiety level. [ABSTRACT FROM AUTHOR]

Individual‐based morphological brain networks built from T1‐weighted magnetic resonance imaging (MRI) reflect synchronous maturation intensities between anatomical regions at the individual level. Autism spectrum disorder (ASD) is a socio‐cognitive and neurodevelopmental disorder with high neuroanatomical heterogeneity, but the specific patterns of morphological networks in ASD remain largely unexplored at the individual level. In this study, individual‐based morphological networks were constructed by using high‐resolution structural MRI data from 40 young children with ASD (age range: 2–8 years) and 38 age‐, gender‐, and handedness‐matched typically developing children (TDC). Measurements were recorded as threefold. Results showed that compared with TDC, young children with ASD exhibited lower values of small‐worldness (i.e., σ) of individual‐level morphological brain networks, increased morphological connectivity in cortico‐striatum‐thalamic‐cortical (CSTC) circuitry, and decreased morphological connectivity in the cortico‐cortical network. In addition, morphological connectivity abnormalities can predict the severity of social communication deficits in young children with ASD, thus confirming an associational impact at the behavioral level. These findings suggest that the morphological brain network in the autistic developmental brain is inefficient in segregating and distributing information. The results also highlight the crucial role of abnormal morphological connectivity patterns in the socio‐cognitive deficits of ASD and support the possible use of the aberrant developmental patterns of morphological brain networks in revealing new clinically‐relevant biomarkers for ASD. [ABSTRACT FROM AUTHOR]

Objective The insula consists of functionally diverse subdivisions, and each division plays different roles in schizophrenia neuropathology. The current study aimed to investigate the abnormal patterns of dynamic functional connectivity (dFC) of insular subdivisions in schizophrenia and the effect of antipsychotics on these connections. Methods Longitudinal study of the dFC of insular subdivisions was conducted in 42 treatment-naive first-episode patients with schizophrenia at baseline and after 8 weeks of risperidone treatment based on resting-state functional magnetic resonance image (fMRI). Results At baseline, patients showed decreased dFC variance (less variable) between the insular subdivisions and the precuneus, supplementary motor area and temporal cortex, as well as increased dFC variance (more variable) between the insular subdivisions and parietal cortex, compared with healthy controls. After treatment, the dFC variance of the abnormal connections were normalized, which was accompanied by a significant improvement in positive symptoms. Conclusions Our findings highlighted the abnormal patterns of fluctuating connectivity of insular subdivision circuits in schizophrenia and suggested that these abnormalities may be modified after antipsychotic treatment. [ABSTRACT FROM AUTHOR]

Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder characterized by substantial clinical and biological heterogeneity. Quantitative and individualized metrics for delineating the heterogeneity of brain structure in ASD are still lacking. Likewise, the extent to which brain structural metrics of ASD deviate from typical development (TD) and whether deviations can be used for parsing brain structural phenotypes of ASD is unclear. T1-weighted magnetic resonance imaging data from the Autism Brain Imaging Data Exchange (ABIDE) II (n TD = 564) were used to generate a normative model to map brain structure deviations of ABIDE I subjects (n TD = 560, n ASD = 496). Voxel-based morphometry was used to compute gray matter volume. Non-negative matrix factorization was employed to decompose the gray matter matrix into 6 factors and weights. These weights were used for normative modeling to estimate the factor deviations. Then, clustering analysis was used to identify ASD subtypes. Compared with TD, ASD showed increased weights and deviations in 5 factors. Three subtypes with distinct neuroanatomical deviation patterns were identified. ASD subtype 1 and subtype 3 showed positive deviations, whereas ASD subtype 2 showed negative deviations. Distinct clinical manifestations in social communication deficits were identified among the three subtypes. Our findings suggest that individuals with ASD have heterogeneous deviation patterns in brain structure. The results highlight the need to test for subtypes in neuroimaging studies of ASD. This study also presents a framework for understanding neuroanatomical heterogeneity in this increasingly prevalent neurodevelopmental disorder. [ABSTRACT FROM AUTHOR]

Abnormalities in the structure of subcortical regions are central to numerous behaviors affected by autism spectrum disorder (ASD), and these regions may undergo atypical coordinated neurodevelopment. However, relatively little is known about morphological correlations among subcortical structures in young children with ASD. In this study, using volumetric-based methodology and structural covariance approach, we investigated structural covariance of subcortical brain volume in 40 young children with ASD (<7.5 years old) and 38 age-, gender-, and handedness-matched typically developing (TD) children. Results showed that compared with TD children, children with ASD exhibited decreased structural covariation between the left and right cerebral hemispheres, specifically between the left and right thalami, right globus pallidus and left nucleus accumbens, and left globus pallidus and right nucleus accumbens. Compared with TD children, children with ASD exhibited increased structural covariation between adjacent regions, such as between the right globus pallidus and right putamen. Additionally, abnormalities in subcortical structural covariance can predict social communication and repetitive and stereotypic behavior in young children with ASD. Overall, these results suggest decreased long-range structural covariation and enhanced local covariation in subcortical structures in children with ASD, highlighting aberrant developmental coordination or synchronized maturation between subcortical regions that play crucial roles in social cognition and behavior in ASD. • Decreased inter-hemispheric structural covariation in ASD. • Increased intra-hemispheric structural covariation in ASD. • Abnormalities in subcortical structural covariance can predict behavior of ASD. [ABSTRACT FROM AUTHOR]