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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.

The Somato-Psychic Pathway (SPP) is proposed as a universal ontogenetic developmental trajectory through which somatic structural–functional integrity and autonomic regulation shape the emergence and stability of the mind under both physiological and pathological conditions. Integrating insights from developmental neuroscience, evolutionary biology, and clinical neurodevelopment, SPP conceptualizes mental functions as interpretive extensions of bodily and autonomic states rather than as their primary generators. The framework delineates a developmentally constrained directional sequence beginning with somatic organization, proceeding through proprioceptive and interoceptive accuracy, and culminating in autonomic regulation, emotional stability, and cognitive–social maturation. Disruption of this trajectory—most prominently through axial dysfunction, distorted joint–muscle–fascial proprioception, persistent low-grade nociceptive drive, or direct mechanical influences on peripheral autonomic structures—is proposed to lead to Somato-Psychic Autonomic Dysregulation (SPAD), a state characterized by chronically reduced autonomic flexibility and heightened threat responsivity. Prolonged operation of the pathway in this pathological mode gives rise to the clinical phenotype termed Somato-Psychic Syndrome (SPS). The SPP framework emerged from longitudinal clinical observation of disrupted and restituted developmental trajectories, providing a unique ontogenetic perspective on the directionality of neurodevelopmental regulation. By integrating the somatic, autonomic, emotional, and cognitive domains into a single regulatory continuum, SPP offers a biologically grounded model with implications for understanding childhood neurodevelopmental disorders and guiding future therapeutic strategies.

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.

Neuroinflammation is instigated by the misfiring of immune cells in the central nervous system (CNS) involving microglia and astrocytes as key cell-types. Neuroinflammation is a consequence of CNS injury, infection, toxicity, or autoimmunity. It is favorable as well as a detrimental process for neurodevelopment and associated processes. Transient activation of inflammatory response involving release of cytokines and growth factors positively affects the development and post-injury tissue. However, chronic or uncontrolled inflammatory responses may lead to various neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis, and multiple sclerosis. These diseases have variable clinical and pathological features, but are underlaid by the aggregation of misfolded proteins with a cytotoxic effect. Notably, abnormal activation of glial cells could mediate neuroinflammation, leading to the neurodegenerative condition. Microglia, a type of glial cell, a resident immune cell, form the forefront defense of the CNS immune system. Dysfunctional microglia and astrocyte, a different kind of glial cell with homeostatic function, impairs the protein aggregate (amyloid-beta plaque) clearance in AD. Studies have shown that microglia and astrocytes undergo alterations in their genetic profile, cellular and molecular responses, and thus promote dysfunctional immune cross-talk in AD. Hence, targeting microglia and astrocytes-driven molecular pathways could resolve the particular layers of neuroinflammation and set a reliable therapeutic intervention in AD progression.

Oculomotor characteristics, including accuracy, timing, and sensorimotor processing, are considered sensitive intermediate phenotypes for understanding the etiology of neurodevelopmental conditions, such as autism and ADHD. Oculomotor characteristics have predominantly been studied separately in autism and ADHD. Despite the high rates of co-occurrence between these conditions, only one study has investigated oculomotor processes among those with co-occurring autism + ADHD. Four hundred and five ( n  = 405; 226 males) Australian children and adolescents aged 4 to 18 years (M = 9.64 years; SD  = 3.20 years) with ADHD ( n  = 64), autism ( n  = 66), autism + ADHD ( n  = 146), or neurotypical individuals ( n  = 129) were compared across four different oculomotor tasks: visually guided saccade, anti-saccade, sinusoidal pursuit and step-ramp pursuit. Confirmatory analyses were conducted using separate datasets acquired from the University of Nottingham UK ( n  = 17 autism, n  = 22 ADHD, n  = 32 autism + ADHD, n  = 30 neurotypical) and University of Kansas USA ( n  = 29 autism, n  = 41 neurotypical). Linear mixed effect models controlling for sex, age and family revealed that children and adolescents with autism + ADHD exhibited increased variability in the accuracy of the final saccadic eye position compared to neurotypical children and adolescents. Autistic children and adolescents demonstrated a greater number of catch-up saccades during step-ramp pursuit compared to neurotypical children and adolescents. These findings suggest that select differences in saccadic precision are unique to autistic individuals with co-occurring ADHD, indicating that measuring basic sensorimotor processes may be useful for parsing neurodevelopment and clinical heterogeneity in autism.