Neurofibromatosis type 1 (NF1) is a genetic disorder that affects brain development and increases the risk for neurodevelopmental conditions, including autism spectrum disorder. Given similar behavioral phenotypes and potential shared neurobiological processes in NF1 and autism spectrum disorder, this study evaluates two markers of brain maturation in youth with NF1 and typically developing youth, including auditory white matter and cortical response latency. Participants, aged 8-12 years, completed a multimodal neuroimaging protocol that included MRI with diffusion tensor imaging of the auditory radiation and magnetoencephalography. Analyses included group comparisons on fractional anisotropy measures of white matter and M50 latency responses from magnetoencephalography and the coupling between fractional anisotropy and M50. Compared to typically developing youth, youth with NF1 did not show maturation in fractional anisotropy or M50 with age and demonstrated shorter M50 auditory response latency. The association between auditory radiation fractional anisotropy and M50 was different in youth with NF1 compared to typically developing youth with youth with NF1 not showing a significant association between fractional anisotropy and M50. Maturation of auditory white matter and auditory cortical response latency is disrupted in NF1 and there is a lack of coupling between structure and function. Longitudinal imaging research is needed to further evaluate neurodevelopment and associations between these immaturities and behavior.

Drugs targeting synaptic RNA m6A methylation regulate synaptic transmission and plasticity in the rat hippocampus.

Impact of catch-up growth on brain structures involved in emotional regulation in preterm children at 2years of age.

Complement contributes to hyperactive behavior in the 16p11.2 hemideletion mouse model.

Combining quasi-static and high frequency experiments for the viscoelastic characterization of porcine brain tissue.

TGFβ signaling is required during human and chick Neural Crest formation.

A community mental health organization's use of decision support dashboards for indicator monitoring: Development and early implementation.

Joint impact of acute stress and alcohol consumption on neurocognition and addiction vulnerability in adolescence and emerging adulthood: A preregistered systematic review.

Disrupted left frontal operculum connectivity in adolescent depression: Mediating the impact of childhood emotional neglect.

Minority and socioeconomically disadvantaged children face disproportionate air pollution burdens, yet the geographic heterogeneity and intersectional structure of these disparities remain poorly characterized in pediatric populations. Using baseline data (2016-2018) from the Adolescent Brain Cognitive Development Study, the largest longitudinal study of child brain development in the United States, we estimated residential fine particulate matter (PM2.5) and nitrogen dioxide (NO2) among 9- to 10-year-olds across 21 sites spanning 19 metropolitan areas. We employed an intersectional analytic approach to examine race/ethnicity and socioeconomic effects jointly, and a two-stage meta-analytic design to explicitly model between-site heterogeneity. Hispanic/Latinx and Black children experienced higher average PM2.5 and NO2 than white peers overall, but intersectional analyses revealed that Hispanic/Latinx preadolescents from the lowest income households bore the greatest PM2.5 burden, and higher educated Black families showed increased NO2 exposure relative to those with high school diplomas. Site-specific analyses revealed substantial geographic heterogeneity in disparity magnitude, challenging the assumption of homogeneous national patterns. These findings underscore the need for locally targeted interventions. Nearly all participants exceeded World Health Organization air quality guidelines despite meeting Environmental Protection Agency thresholds, highlighting a regulatory gap with particular relevance to children's developing neurological systems.

Pubertal timing predicts resting-state functional connectivity of cortical networks.

Neurodevelopmental markers in psychiatric disorders: A systematic review of facial dysmorphology assessed through 3D based-morphometric methods.

Attention-deficit/hyperactivity disorder (ADHD) is a common neurodevelopmental condition with multifactorial etiology involving genetic, neurobiological, and environmental determinants. Emerging evidence suggests that environmental exposures may influence neurodevelopmental pathways relevant to ADHD pathophysiology. Manganese is an essential trace element required for normal brain development; however, excessive or dysregulated exposure has been associated with neurotoxic effects. This systematic review aimed to synthesize human evidence on the association between manganese exposure and ADHD or ADHD-related neurobehavioral outcomes in children. Four electronic databases were systematically searched according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Observational studies meeting predefined Population, Exposure, Comparison, Outcomes, and Study Design criteria were included. Methodological quality was assessed using Joanna Briggs Institute appraisal tools, and certainty of evidence was evaluated using the Grading of Recommendations, Assessment, Development, and Evaluation framework. Thirty studies met the inclusion criteria. Elevated manganese exposure was more frequently associated with increased risk or severity of ADHD or ADHD-related neurobehavioral symptoms, although inverse and nonlinear (U-shaped) associations were also reported. The available evidence indicates a complex and potentially nonlinear relationship between manganese exposure and child neurobehavioral outcomes. These findings identify manganese exposure as a potentially modifiable environmental factor influencing neurodevelopmental mechanisms relevant to ADHD and highlight the need for longitudinal studies integrating exposure biomarkers with neurobiological and clinical outcomes to clarify causal pathways and therapeutic implications.

Modeling sporadic Alzheimer's disease using brain organoids: Emerging trends and translational opportunities.

PTBP1: A master regulator of neural development and transdifferentiation-promise and pitfalls.

The gut-brain axis and trimethylamine N-oxide: an emergent biomarker in neurological diseases.

HMGA2 regulates fear and growth: Canine GWAS and functional evidence.

Single-cell RNA sequencing reveals cadmium-induced cell-type-specific mechanisms of developmental neurotoxicity in human cortical organoids.

Prenatal and early-life exposure to micro- and nanoplastics and autism-relevant neurodevelopment: An integrated review of human, experimental, and mechanistic evidence.

To explore the clinical phenotype and genetic etiology of a fetus with autosomal dominant intellectual disability type 72 (MRD72) resulting from a variant of the SRRM2 gene. A Chinese pedigree with MRD72 (fetus) who had visited the Affiliated Women and Children's Hospital of Ningbo University in November 2024 was selected as study subject. Clinical data of the pedigree were collected. Amniotic fluid and peripheral blood samples were collected from the fetus and its parents for genomic DNA extraction. Whole-exome sequencing (WES) was carried out, and candidate variants were verified by Sanger sequencing of the family members and rated based on guidelines from the American College of Medical Genetics and Genomics (ACMG). Relevant literature on MRD72 were searched in domestic and international databases for a review. This study was approved by the hospital (Ethics No.: EC2023-094). The proband was a fetus of 25 weeks of gestation. Fetal echocardiography revealed a relatively small left atrium and left ventricle, along with a diminished aortic-to-pulmonary artery ratio. WES revealed that the fetus has harbored a heterozygous nonsense variant of the SRRM2 gene. Sanger sequencing confirmed both parents carried the wild-type alleles. Based on guidelines from the American College of Medical Genetics and Genomics (ACMG), the variant was rated as likely pathogenic (PVS1+PM2_Supporting) and has not been recorded in public databases. Bioinformatic analysis predicted amino acid 512 to be highly conserved across various species. According to the pre-set literature search strategy, 4 publications were retrieved, which involved 30 MRD72 patients from 27 pedigrees, In addition to this study, a total of 31 cases were included. Analysis of clinical features and genetic etiology showed that patients with MRD72 presented mainly with clinical manifestations such as mental and motor development delay, special facial features, speech/intellectual development delay, and obesity. The genetic etiology was all variants at relevant loci of the SRRM2 gene. The SRRM2 variant identified in this study is implicated as the genetic cause of MRD72 in the proband. Above results have expanded the mutational and phenotypic spectra of the SRRM2 gene.