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We offer an integrative perspective on how the air-pollution exposome shapes fetal development during the first 1,000 days and reverberates across mental health and behavior. Pregnant individuals and young children are disproportionately exposed to particulate matter (PM2.5), nitrogen dioxide (NO 2 ), ozone (O 3 ), and volatile organic compounds (VOCs) with social disadvantage amplifying risk. We bridge exposure to biology through three conduits. First, the placenta acts as a sensor and recorder, transducing signals that alter growth, immune tone, and neuroendocrine programming. Second, fetal autonomic control–captured by beat-to-beat fetal heart rate variability (fHRV) offers a relevant biomarker of neurodevelopmental integrity; the absence of direct ambient-pollution–fHRV studies is a pressing gap. Third, maternal immune activation, oxidative and endoplasmic reticulum (ER) stress, and disrupted morphogenesis reshape developing circuits, changes now traceable in utero by advanced fetal MRI. These pathways fit a developmental-programming frame: epigenetic remodeling, gene–environment interplay, endocrine-disrupting co-exposures, and gut-microbiome shifts create durable susceptibility. Clinically, the result is structural and functional brain alterations and child phenotypes spanning attention, executive control, affecting regulation, and learning, with clear pediatric and educational implications. We propose an exposome-based research agenda coupling high-resolution exposure assessment with placental molecular profiling, fetal/neonatal autonomic biomarkers (including fHRV), fetal/child neuroimaging, and longitudinal microbiome readouts in harmonized cohorts. In parallel, multisectoral actions–clean air urban design, targeted protection of pregnancy and early childhood, chemical regulation, and risk communication–should narrow exposure inequities while trials test biomarker-guided prevention. Aligning placental biology, autonomic metrics, and exposome science may transform risk stratification and safeguard the developing brain.

Fossil-fuel combustion by-products are the world’s most significant threat to children’s health and future and are major contributors to global inequality and environmental injustice. The emissions include a myriad of toxic air pollutants and carbon dioxide (CO2), which is the most important human-produced climate-altering greenhouse gas. Synergies between air pollution and climate change can magnify the harm to children. Impacts include impairment of cognitive and behavioral development, respiratory illness, and other chronic diseases—all of which may be “seeded“ in utero and affect health and functioning immediately and over the life course. By impairing children’s health, ability to learn, and potential to contribute to society, pollution and climate change cause children to become less resilient and the communities they live in to become less equitable. The developing fetus and young child are disproportionately affected by these exposures because of their immature defense mechanisms and rapid development, especially those in low- and middle-income countries where poverty and lack of resources compound the effects. No country is spared, however: even high-income countries, especially low-income communities and communities of color within them, are experiencing impacts of fossil fuel-related pollution, climate change and resultant widening inequality and environmental injustice. Global pediatric health is at a tipping point, with catastrophic consequences in the absence of bold action. Fortunately, technologies and interventions are at hand to reduce and prevent pollution and climate change, with large economic benefits documented or predicted. All cultures and communities share a concern for the health and well-being of present and future children: this shared value provides a politically powerful lever for action. The purpose of this commentary is to briefly review the data on the health impacts of fossil-fuel pollution, highlighting the neurodevelopmental impacts, and to briefly describe available means to achieve a low-carbon economy, and some examples of interventions that have benefited health and the economy.

Background Infant neurodevelopment in the first years after birth is determined by multiple factors, including parental care and maternal mental wellbeing. In this study, we aim to assess the impact of persistent maternal depressive symptoms during the first 3 months postpartum on infant neurodevelopment at 6 months. Methods Using a longitudinal cohort design, 1253 mother-infant pairs were followed up at 7, 45, and 90 days to assess postpartum depressive symptoms using the Edinburgh Postnatal Depression Scale (EPDS); infants were followed up at 6 months to assess neuro-developmental status using the WHO’s Infant and Young Child Development (IYCD) tool. A generalized linear regression model was used to assess the association between persistent postpartum depressive symptoms and infant neurodevelopmental delay at 6 months. A generalized linear mixed model (GLMM) with a hospital as a random intercept was used to assess the persistent postpartum depressive symptoms with an IYCD score. Linear regression was used to compare the IYCD scores between exposure groups. Results In the study population, 7.5% of mothers had persistent depressive symptoms, and 7.5% of infants had neurodevelopmental delay. Infants born to mothers with persistent depressive symptoms had a higher proportion of neurodevelopmental delay than infants born to women without persistent symptoms (48.6% vs 5.1%; p  < 0.001). In the adjusted regression model, infants whose mothers had persistent depressive symptoms at 7, 45, and 90 days had a 5.21-fold increased risk of neurodevelopmental delay (aRR, 5.21; 95% CI, 3.17, 8.55). Mean scores in the motor domain (12.7 vs 15.2; p  < 0.001) and language domain (6.4 vs 8.5; p  < 0.001) were significant when a mother had persistent depression vs. no depression. Mean scores in the general behavioral domain (5.9 vs 10.4, p  < 0.001) and the socio-emotional domain (15.4 vs 17.7; p  < 0.001) were significantly different when a mother had persistent depression vs no persistent depression. Conclusions Our results suggest that 6-month-old infants are at higher risk for neurodevelopment delays if their mother reports persistent symptoms of depression from 7 to 90 days postpartum. The neurodevelopmental delay can be observed in all functional domains. Preventive intervention to reduce maternal postpartum depression may reduce the impact on infant developmental delay.

The blood-brain barrier (BBB) maintains brain homeostasis and limits the entry of toxins and pathogens into the brain. Despite its importance, little is known about the molecular mechanisms regulating the development and function of this crucial barrier. In this study we have developed methods to highly purify and gene profile endothelial cells from different tissues, and by comparing the transcriptional profile of brain endothelial cells with those purified from the liver and lung, we have generated a comprehensive resource of transcripts that are enriched in the BBB forming endothelial cells of the brain. Through this comparison we have identified novel tight junction proteins, transporters, metabolic enzymes, signaling components, and unknown transcripts whose expression is enriched in central nervous system (CNS) endothelial cells. This analysis has identified that RXRalpha signaling cascade is specifically enriched at the BBB, implicating this pathway in regulating this vital barrier. This dataset provides a resource for understanding CNS endothelial cells and their interaction with neural and hematogenous cells.

This review article describes the main clinical, emotional, educational, and social aspects involved in the transition to adolescence for individuals with these conditions. It also addresses implications for healthcare, the continuity of educational support, and the importance of individualized transition strategies, highlighting the need for a multidisciplinary approach centered on the individual and on continuity of care. Review of the latest literature on neurodevelopmental disorders in adolescents. Adolescence represents a vital period of biopsychosocial transformation, particularly challenging for individuals with neurodevelopmental disorders (NDDs), such as autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), and intellectual disability. Integrated, person-centered, continuous, and collaborative health care is essential to promote the well-being and inclusion of these adolescents.

BackgroundThe associations between analgesia and/or sedation exposure and adverse outcomes in very preterm infants remain controversial. Evidence linking these medications to moderate-to-severe bronchopulmonary dysplasia (BPD) and long-term neurodevelopmental outcomes is particularly limited in large Chinese preterm cohorts.ObjectiveThe primary aim was to investigate the associations between exposure to analgesia/sedation and the composite outcome of BPD or death. The secondary aim was to assess the association with neurodevelopmental outcomes at 18 months.MethodsThis large, retrospective cohort study included preterm infants (gestational age < 32 weeks) admitted to a tertiary NICU in Shanghai, China, from 2018 to 2022. The primary outcomes were two composite measures: (1) moderate-to-severe BPD or death, and (2) any BPD or death, both assessed at 36 weeks postmenstrual age. The secondary outcomes included neurodevelopmental outcomes at 18 months and key neonatal morbidities. Propensity score matching (PSM) followed by multivariable logistic regression was used to adjust for confounders.ResultsOf the 713 infants included in the primary analysis, 116 (16.3%) were exposed to analgesia/sedation. In the PSM cohort (n = 460), after multivariable adjustment, exposure was associated with a significantly increased risk of moderate-to-severe BPD or death (adjusted OR, 6.00; 95% CI, 3.35–10.74; p < 0.001) and any BPD or death (adjusted OR, 5.32; 95% CI, 3.15–8.98; p < 0.001). Furthermore, the exposure group experienced significantly longer durations of invasive mechanical ventilation (IMV), higher incidences of hypotension requiring intervention and feeding intolerance (all p < 0.05). In a separate analysis of the matched neurodevelopmental subcohort (n = 129), no significant associations were found with neurodevelopmental outcomes at 18 months.ConclusionIn this large Chinese preterm cohort, analgesia/sedation exposure was significantly associated with an increased risk of BPD or death. This association was observed alongside a series of neonatal morbidities such as prolonged IMV and hemodynamic instability, though no significant long-term neurodevelopmental harm was detected at 18 months.

Rare coding variation has historically provided the most direct connections between gene function and disease pathogenesis. By meta-analysing the whole exomes of 24,248 schizophrenia cases and 97,322 controls, we implicate ultra-rare coding variants (URVs) in 10 genes as conferring substantial risk for schizophrenia (odds ratios of 3–50, P  < 2.14 × 10 −6 ) and 32 genes at a false discovery rate of <5%. These genes have the greatest expression in central nervous system neurons and have diverse molecular functions that include the formation, structure and function of the synapse. The associations of the NMDA ( N -methyl- d -aspartate) receptor subunit GRIN2A and AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptor subunit GRIA3 provide support for dysfunction of the glutamatergic system as a mechanistic hypothesis in the pathogenesis of schizophrenia. We observe an overlap of rare variant risk among schizophrenia, autism spectrum disorders 1 , epilepsy and severe neurodevelopmental disorders 2 , although different mutation types are implicated in some shared genes. Most genes described here, however, are not implicated in neurodevelopment. We demonstrate that genes prioritized from common variant analyses of schizophrenia are enriched in rare variant risk 3 , suggesting that common and rare genetic risk factors converge at least partially on the same underlying pathogenic biological processes. Even after excluding significantly associated genes, schizophrenia cases still carry a substantial excess of URVs, which indicates that more risk genes await discovery using this approach. Whole-exome sequencing identifies ten risk genes for schizophrenia implicated by rare protein-coding variants, a subset of which overlap with risk genes in other neurodevelopmental disorders.

The gut microbiota has been found to interact with the brain through the microbiota-gut-brain axis, regulating various physiological processes. In recent years, the impacts of the gut microbiota on neurodevelopment through this axis have been increasingly appreciated. The gut microbiota is commonly considered to regulate neurodevelopment through three pathways, the immune pathway, the neuronal pathway, and the endocrine/systemic pathway, with overlaps and crosstalks in between. Accumulating studies have identified the role of the microbiota-gut-brain axis in neurodevelopmental disorders including autism spectrum disorder, attention deficit hyperactivity disorder, and Rett Syndrome. Numerous researchers have examined the physiological and pathophysiological mechanisms influenced by the gut microbiota in neurodevelopmental disorders (NDDs). This review aims to provide a comprehensive overview of advancements in research pertaining to the microbiota-gut-brain axis in NDDs. Furthermore, we analyzed both the current state of research progress and discuss future perspectives in this field.