Brain Development Research Articles

NLRP3 inflammasome-mitochondrion loop in autism spectrum disorder

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by deficits in social communication and the presence of restricted interests and repetitive behavior. To date, no single cause has been demonstrated but both genetic and environmental factors are believed to be involved in abnormal brain development. In recent years, immunological and mitochondrial dysfunctions acquired particular interest in the study of the molecular mechanisms underlying the pathophysiology of ASD. For this reason, our study focused on evaluating the mitochondrial component and activation of the NLRP3 inflammasome, a critical player of the innate immune system. The assembly of NLRP3 with ASC mediates activation of Caspase-1, which in turn, by proteolytic cleavage, activates Gasdermin D and the proinflammatory cytokines IL-1β/IL-18 with their subsequent secretion. Using primary fibroblasts of autistic and control patients we studied basal and stimulated conditions. Specifically, LPS and ATP were used to activate the NLRP3 inflammasome and MCC950 for its inhibition. In addition, FCCP was used as a mitochondrial stressor and MitoTEMPO as a scavenger of mitochondrial ROS. Our results showed a hyperactivation of NLRP3 inflammasome in ASDs, as evidenced by the co-localization of the two main components, NLRP3 and ASC, by the higher levels of ASC specks, oligomers and dimers and by the increased amounts of active Caspase-1 and IL-1β. In addition, increased mitochondrial superoxide anion and reduced mitochondrial membrane potential were detected in ASD cells. These data are in accordance with the abnormal mitochondrial morphology evidenced by transmission electron microscopy analysis. Interestingly, NLRP3 inflammasome inhibition with MCC950 improved mitochondrial parameters, while the use of MitoTEMPO, in addition to decrease mitochondrial ROS production, was able to prevent NLRP3 inflammasome activation suggesting for the first time an abnormal bidirectional crosstalk between mitochondria and NLRP3 inflammasome in ASD.

The role of multisensory intervention combined with aEEG in the maturation and evaluation of brain and neural development in premature infants of different gestational ages

Objective: To explore the combined effects of multisensory intervention and amplitude integrated electroencephalogram monitoring on the maturation and evaluation of brain and neural development in premature infants of different gestational ages.Methods: The controlled trial was carried out in 62 premature infants from January to February of 2023 in Genertec AMHT – Baogang Hospital. The premature infants were divided into two groups according to the gestational age: 32-33+6W (Group A) and 34-33+6W (Group B). By use of random number table method, each group was subdivided into the control group and the experimental group. The control group was monitored with aEEG within 1 day and the following 7 days after birth. The experimental group was monitored with aEEG within 1 day and the following 7 days after multisensory intervention (MS) to observe the change of aEEG parameters, in order to explore the effect of MS intervention on brain development maturity. The Neonatal Behavioral Neurological Assessment (NBNA) score was performed at 40 weeks of corrected gestational age in both groups.Results: The amplitude voltage, the total aEEG score and the sleep-wake cycle score in the experimental group were higher than those in the control group (p < .05). The total NBNA score in the experimental group was higher than that in the control group.Conclusion: The multi-sensory intervention is a simple and feasible method of development support nursing, it can improve the total NBNA score of premature infants, which can promote the brain development in premature infants and improve their neurodevelopmental behavior.

Population clustering of structural brain aging and its association with brain development

Structural brain aging has demonstrated strong inter-individual heterogeneity and mirroring patterns with brain development. However, due to the lack of large-scale longitudinal neuroimaging studies, most of the existing research focused on the cross-sectional changes of brain aging. In this investigation, we present a data-driven approach that incorporate both cross-sectional changes and longitudinal trajectories of structural brain aging and identified two brain aging patterns among 37,013 healthy participants from UK Biobank. Participants with accelerated brain aging also demonstrated accelerated biological aging, cognitive decline and increased genetic susceptibilities to major neuropsychiatric disorders. Further, by integrating longitudinal neuroimaging studies from a multi-center adolescent cohort, we validated the ‘last in, first out’ mirroring hypothesis and identified brain regions with manifested mirroring patterns between brain aging and brain development. Genomic analyses revealed risk loci and genes contributing to accelerated brain aging and delayed brain development, providing molecular basis for elucidating the biological mechanisms underlying brain aging and related disorders.

Population clustering of structural brain aging and its association with brain development.

Structural brain aging has demonstrated strong inter-individual heterogeneity and mirroring patterns with brain development. However, due to the lack of large-scale longitudinal neuroimaging studies, most of the existing research focused on the cross-sectional changes of brain aging. In this investigation, we present a data-driven approach that incorporate both cross-sectional changes and longitudinal trajectories of structural brain aging and identified two brain aging patterns among 37,013 healthy participants from UK Biobank. Participants with accelerated brain aging also demonstrated accelerated biological aging, cognitive decline and increased genetic susceptibilities to major neuropsychiatric disorders. Further, by integrating longitudinal neuroimaging studies from a multi-center adolescent cohort, we validated the 'last in, first out' mirroring hypothesis and identified brain regions with manifested mirroring patterns between brain aging and brain development. Genomic analyses revealed risk loci and genes contributing to accelerated brain aging and delayed brain development, providing molecular basis for elucidating the biological mechanisms underlying brain aging and related disorders.

Corticostriatal Maldevelopment in the R6/2 Mouse Model of Juvenile Huntington's Disease.

There is a growing consensus that brain development in Huntington's disease (HD) is abnormal, leading to the idea that HD is not only a neurodegenerative but also a neurodevelopmental disorder. Indeed, structural and functional abnormalities have been observed during brain development in both humans and animal models of HD. However, a concurrent study of cortical and striatal development in a genetic model of HD is still lacking. Here we report significant alterations of corticostriatal development in the R6/2 mouse model of juvenile HD. We examined wildtype (WT) and R6/2 mice at postnatal (P) days 7, 14, and 21. Morphological examination demonstrated early structural and cellular alterations reminiscent of malformations of cortical development, and ex vivo electrophysiological recordings of cortical pyramidal neurons (CPNs) demonstrated significant age- and genotype-dependent changes of intrinsic membrane and synaptic properties. In general, R6/2 CPNs had reduced cell membrane capacitance and increased input resistance (P7 and P14), along with reduced frequency of spontaneous excitatory and inhibitory synaptic events during early development (P7), suggesting delayed cortical maturation. This was confirmed by increased occurrence of GABA A receptor-mediated giant depolarizing potentials at P7. At P14, the rheobase of CPNs was significantly reduced, along with increased excitability. Altered membrane and synaptic properties of R6/2 CPNs recovered progressively, and by P21 they were similar to WT CPNs. In striatal medium-sized spiny neurons (MSNs), a different picture emerged. Intrinsic membrane properties were relatively normal throughout development, except for a transient increase in membrane capacitance at P14. The first alterations in MSNs synaptic activity were observed at P14 and consisted of significant deficits in GABAergic inputs, however, these also were normalized by P21. In contrast, excitatory inputs began to decrease at this age. We conclude that the developing HD brain is capable of compensating for early developmental abnormalities and that cortical alterations precede and are a main contributor of striatal changes. Addressing cortical maldevelopment could help prevent or delay disease manifestations.

Enhancing daily life for children with cognitive developmental delay through insights into brain development.

Cognitive developmental delay, including severe intellectual disability (IQ below 70) and borderline intellectual functioning (IQ 70-85), poses significant challenges, including high costs and emotional burden. Early diagnosis and interventions might improve adaptive behavior and daily life functioning. High-risk groups include children with neonatal complications, congenital anomalies, genetic disorders, or metabolic errors, yet over 50% of cases have unknown causes. To provide timely diagnosis and intervention for children with cognitive developmental delay, it is important to increase our understanding and ability to prognosticate their level of functioning. The pivotal role of brain development in the first few years of life presents a window of opportunity for these goals. By detailed investigation of common patterns in structural brain development and connectivity by MRI in relation to cognitive and executive functioning, this review aims to identify potential factors that might improve understanding and prognostication of children with cognitive developmental delay. Exploring similarities among diverse patient groups with childhood cognitive developmental delay, this review intends to provide a nuanced perspective. IMPACT: This review identified several MRI brain developmental markers, especially in the white matter, that might hold potential to be a prognostic marker for intellectual and executive functioning in children with cognitive developmental delay. Bringing together information on aberrant brain developmental trajectories and connectivity across different patient childhood populations with cognitive developmental delay might improve our understanding and prognostication.

MAPbrain: a multi-omics atlas of the primate brain.

The brain is the central hub of the entire nervous system. Its development is a lifelong process guided by a genetic blueprint. Understanding how genes influence brain development is critical for deciphering the formation of human cognitive functions and the underlying mechanisms of neurological disorders. Recent advances in multi-omics techniques have now made it possible to explore these aspects comprehensively. However, integrating and analyzing extensive multi-omics data presents significant challenges. Here, we introduced MAPbrain (http://bigdata.ibp.ac.cn/mapBRAIN/), a multi-omics atlas of the primate brain. This repository integrates and normalizes both our own lab's published data and publicly available multi-omics data, encompassing 21 million brain cells from 38 key brain regions and 436 sub-regions across embryonic and adult stages, with 164 time points in humans and non-human primates. MAPbrain offers a unique, robust, and interactive platform that includes transcriptomics, epigenomics, and spatial transcriptomics data, facilitating a comprehensive exploration of brain development. The platform enables the exploration of cell type- and time point-specific markers, gene expression comparison between brain regions and species, joint analyses across transcriptome and epigenome, and navigation of cell types across species, brain regions, and development stages. Additionally, MAPbrain provides an online integration module for users to navigate and analyze their own data within the platform.

Sports and activity games as a means of increasing the motive activity of educators

At the current stage, the problem of insufficient movement mode of the participants of the educational process, which negatively affects their physical development and the state of mental processes, in particular: feeling, perception, thinking, memorization, attention, needs special attention. This fact reduces the success of studies to some extent. Therefore, it is necessary to look for ways to use such means of motor activity that would contribute to the improvement of the physical and psychological condition of students. The goal is to reveal the peculiarities of the use of mobile and sports games in the educational process of physical education in higher education institutions as a means of improving the motor activity of students. Research results. The expediency of using the sports and game method in the process of physical education of students, which provides sufficient physical activity and contributes to strengthening health, forms moral and willpower qualities of the individual, is revealed. A rich arsenal of sports games, including basketball, volleyball, mini-football, their nature, structure and intensity are highlighted. It is noted that with the help of sports games, students develop important physical qualities: strength, speed, dexterity, endurance, consolidate and improve various skills and abilities in walking, running, jumping. Attention is paid to the careful selection of mobile games, taking into account the physical fitness and interests of students, their capabilities, which will make it possible to diversify classes and form the necessary motor skills. Conclusions. The use of the sports and game method in physical education classes contributes to the comprehensive development of the student's personality, as it causes positive emotions, a sense of satisfaction, cheerfulness, activity, and has a positive effect on physical and mental development.

Cannabis and Cannabinoid Signaling: Research Gaps and Opportunities.

Cannabis and its products have been used for centuries for both medicinal and recreational purposes. The recent widespread legalization of cannabis has vastly expanded its use in the United States across all demographics except for adolescents. Meanwhile, decades of research have advanced our knowledge of cannabis pharmacology and particularly of the endocannabinoid system with which the components of cannabis interact. This research has revealed multiple targets and approaches for manipulating the system for therapeutic use and to ameliorate cannabis toxicity or cannabis use disorder. Research has also led to new questions that underscore the potential risks of its widespread use, particularly the enduring consequences of exposure during critical windows of brain development or for consumption of large daily doses of cannabis with high content Δ 9-tetrahydrocannabinol. This article highlights current neuroscience research on cannabis that has shed light on therapeutic opportunities and potential adverse consequences of misuse and points to gaps in knowledge that can guide future research. SIGNIFICANCE STATEMENT: Cannabis use has escalated with its increased availability. Here, the authors highlight the challenges of cannabis research and the gaps in our knowledge of cannabis pharmacology and of the endocannabinoid system that it targets. Future research that addresses these gaps is needed so that the endocannabinoid system can be leveraged for safe and effective use.

Phase-Specific Immobilization of Phospholipase D as an Efficient Pickering Emulsion Interfacial Catalyst for Converting Antarctic Krill Oil Phospholipid.

Phosphatidylserine (PS), a rare phospholipid in Antarctic krill oil (AKO) critical for brain development, can be produced from the abundant phosphatidylcholine (PC) using phospholipase D (PLD) in Pickering emulsion interfacial catalysis (PIC) systems. However, the exposure of PLD to organic solvent around the emulsion interface diminished PLD activity, limiting the conversion efficiency of PS. In this study, we proposed a strategy to fabricate a PIC system with high efficiency and stability by immobilizing PLD in a specific phase on the emulsion interface, based on investigating the effect of the interfacial microenvironment on PLD activity. Janus-poly(acrylic acid)/polystyrene (JPP) and Janus-polyethylenimine/octadecane (JPO) particles were fabricated as carriers to realize the specific-phase immobilization of PLD. The highest activity was observed when PLD was immobilized on the hydrophilic side of JPP (PLD@JPP(W)), 1.9-fold that of free PLD. The catalytic efficiency of PLD@JPP(W) was 1.7-fold that of free PLD, confirmed by the kcat/Km value enhancement. Immobilization on the hydrophilic side also enhanced the thermal stability of PLD. The half-lives of PLD were extended from 4 to 36 h at 40 °C and from 6 to 28 days at 4 °C. Importantly, PLD@JPP(W) showed excellent catalytic efficiency as a PIC system, achieving a PS productivity of 93% within a short time of 2 h at an enzyme dosage of 0.05 mg. PLD@JPP(W) exhibited a 3.6 times higher yield than free PLD in the production of PS from PC rich in Antarctic krill oil. The strategy in this work could also be applied to other lipases, providing a promising method for the efficient conversion of functional lipids.

Thyroid-stimulating hormone (TSH) mediates the associations between maternal metals and neurodevelopment in children: A prospective cohort study

Insufficient research has focused on the effects of metal mixtures on children's neurodevelopment and TSH's potential mediating effect. Plasma concentrations of ten metals were measured among 2887 pregnant women in a persistent Chinese birth cohort. At age two, children's neurodevelopment was assessed using mental development indexes (MDIs) and psychomotor development indexes (PDIs), defining neurodevelopmental delay as MDI≤ 79 (cognitive delay) or PDI≤ 79 (motor delay). The associations between single and mixed metals with neurodevelopment delay risk were examined using generalized linear regression complemented by weighted quantile sum (WQS) regression. To investigate the mediated effects of infant Thyroid-Stimulating Hormone (TSH) on metal-associated neurodevelopment delay risk, mediation analyses were conducted. According to the single-metal model, V, Mn, and Pb levels are positively associated with neurodevelopment delay. The WQS model found consistent associations (Odds Ratio [OR] 1.55, 95% Confidence Interval [CI] 1.23 to 1.95), highlighting V, Mn, and Pb as the main causes of cognitive delay. Further mediation analysis revealed that the association between metals (mainly V, Mn, and Pb) and neurodevelopment delay risk is mediated by TSH, with proportions ranging from 3.18 to 10.14% (all P < 0.05). Our findings highlighted prenatal exposure to metals was associated with higher risks of neurodevelopmental delay, with TSH possibly mediating this effect.

SUMOylation of Warts kinase promotes neural stem cell reactivation

A delicate balance between neural stem cell (NSC) quiescence and proliferation is important for adult neurogenesis and homeostasis. Small ubiquitin-related modifier (SUMO)-dependent post-translational modifications cause rapid and reversible changes in protein functions. However, the role of the SUMO pathway during NSC reactivation and brain development is not established. Here, we show that the key components of the SUMO pathway play an important role in NSC reactivation and brain development in Drosophila. Depletion of SUMO/Smt3 or SUMO conjugating enzyme Ubc9 results in notable defects in NSC reactivation and brain development, while their overexpression leads to premature NSC reactivation. Smt3 protein levels increase with NSC reactivation, which is promoted by the Ser/Thr kinase Akt. Warts/Lats, the core protein kinase of the Hippo pathway, can undergo SUMO- and Ubc9-dependent SUMOylation at Lys766. This modification attenuates Wts phosphorylation by Hippo, leading to the inhibition of the Hippo pathway, and consequently, initiation of NSC reactivation. Moreover, inhibiting Hippo pathway effectively restores the NSC reactivation defects induced by SUMO pathway inhibition. Overall, our study uncovered an important role for the SUMO-Hippo pathway during Drosophila NSC reactivation and brain development.

Chromatin remodeller Chd7 is developmentally regulated in the neural crest by tissue-specific transcription factors.

Neurocristopathies such as CHARGE syndrome result from aberrant neural crest development. A large proportion of CHARGE cases are attributed to pathogenic variants in the gene encoding CHD7, chromodomain helicase DNA binding protein 7, which remodels chromatin. While the role for CHD7 in neural crest development is well documented, how this factor is specifically up-regulated in neural crest cells is not understood. Here, we use epigenomic profiling of chick and human neural crest to identify a cohort of enhancers regulating Chd7 expression in neural crest cells and other tissues. We functionally validate upstream transcription factor binding at candidate enhancers, revealing novel epistatic relationships between neural crest master regulators and Chd7, showing tissue-specific regulation of a globally acting chromatin remodeller. Furthermore, we find conserved enhancer features in human embryonic epigenomic data and validate the activity of the human equivalent CHD7 enhancers in the chick embryo. Our findings embed Chd7 in the neural crest gene regulatory network and offer potentially clinically relevant elements for interpreting CHARGE syndrome cases without causative allocation.

Urban Green Infrastructures and Its Impacts on the Urban Environment: A Review

Urban green infrastructure plays a crucial role in preserving a green urban environment, thus contributing significantly to human health. The absence of such infrastructure can lead to environmental challenges, particularly in the face of escalating global urbanization. Green urban infrastructure proves essential for maintaining cleanliness in urban areas, especially as major cities worldwide grapple with escalating air pollution exacerbated by the inadequate presence of green spaces, green roofs, green walls, and domestic and private gardens emerge as noteworthy contributors to mitigating these challenges. As the global population steadily increases, a collective effort is imperative to enhance green infrastructure and cultivate public awareness to address the pressing issue of air pollution in cities. Green spaces serve as a pivotal indicator of urban verdancy, offering a myriad of benefits, including environmental cleanliness, the creation of recreational spaces, the promotion of health and well-being, the facilitation of children’s mental development, the presentation of aesthetically pleasing urban landscapes, temperature reduction, and pollution mitigation. This comprehensive review analyzed 60-70 studies on urban green infrastructures and their impacts on the urban environment. A library research methodology was used, focusing on literature from Google Scholar published in the last two decades which delves into the multifaceted aspects of urban environmental cleanliness, providing valuable insights for policymakers, and urban planners with a profound understanding of their impacts. Stakeholders can proactively implement measures to enhance cleanliness in the urban environment.

CLINICAL AND MOLECULAR CHARACTERIZATION OF A PATIENT WITH SYNDROMIC CRANIOSYNOSTOSIS, A CASE REPORT

Introduction: Craniosynostosis is a craniofacial disorder characterized by premature fusion of one or more cranial sutures, inhibiting bone growth perpendicular to the affected suture. In syndromic craniosynostosis, anomalies of the limbs, heart and central nervous system may be present, in addition to genetic mutations affecting the cranial vault. Its etiology is associated with paternal age, teratogenic factors and external pressure on the skull; the main genes causing syndromic craniosynostosis are the growth factor receptors (FGFR1, FGFR2, and FGFR3, TWIST1 and EFNB1), for these reasons it is of utmost importance to recognize the existing types of syndromic craniosynostosis, and its clinical and molecular characteristics to reach an optimal and accurate diagnosis. Objective: to present the clinical and molecular characterization of an individual with syndromic craniosynostosis in a case. Methodology:an objective description of the clinical case and a review with analysis of a total of 24 articles, including review and original articles, as well as clinical cases, of which 18 bibliographies were used because the other articles were not relevant to this study. The sources of information were indexed journals as well as search engines such as PubMed, Google Scholar and Cochrane; the terms used to search for information were: syndrome, craniosynostosis, gene, mutation, FGFR. Results: the present report shows a clinical case of syndromic craniosynostosis. The diagnosis was made during an evaluation by means of radiographic analysis in a 15-year-old female patient, and corroborated by genetic blood tests with the following results: heterozygous variant at position 755 of the c.DNA, where a variant in Cytosine is visualized by a Guanine. This determines a change at the level of the FGFR2 protein. Conclusions: the case report describes the clinical and molecular diagnosis of a 15-year-old female patient, revealing a heterozygous genetic variant in the FGFR2 gene (c.755&gt;G), associated with changes in the FGFR2 protein. This finding is relevant, as similar variants have not been reported in Ecuador or South America, underscoring the need for further research on syndromic craniosynostosis and Apert syndrome. A multidisciplinary approach to treatment is recommended, involving various medical specialties to ensure proper brain development and improved esthetics. In addition, the existence of similar cases in Indonesia and Congo is mentioned, suggesting a possible founder effect related to the migration of people with character. KEY WORDS: syndrome, craniosynostosis, gene, mutation, FGFR

Spatiotemporal cerebral blood flow dynamics underlies emergence of the limbic-sensorimotor-association cortical gradient in human infancy

Infant cerebral blood flow (CBF) delivers nutrients and oxygen to fulfill brain energy consumption requirements for the fastest period of postnatal brain development across the lifespan. However, organizing principle of whole-brain CBF dynamics during infancy remains obscure. Leveraging a unique cohort of 100+ infants with high-resolution arterial spin labeled MRI, we find the emergence of the cortical hierarchy revealed by the highest-resolution infant CBF maps available to date. Infant CBF across cortical regions increases in a biphasic pattern featured by initial rapid and subsequently slower rate, and break-point ages increasing along the limbic-sensorimotor-association cortical gradient. Increases in CBF in sensorimotor cortices are associated with enhanced language and motor skills, and frontoparietal association cortices with cognitive skills. The study discovers emergence of the hierarchical limbic-sensorimotor-association cortical gradient in infancy and offers standardized reference of infant brain CBF and insight into the physiological basis of cortical specialization and real-world infant developmental functioning.

Sex Differences in Human Brain Structure at Birth

BackgroundSex differences in human brain anatomy have been well-documented, though remain significantly underexplored during early development. The neonatal period is a critical stage for brain development and can provide key insights into the role that prenatal and early postnatal factors play in shaping sex differences in the brain.MethodsHere, we assessed on-average sex differences in global and regional brain volumes in 514 newborns aged 0–28 days (236 birth-assigned females and 278 birth-assigned males) using data from the developing Human Connectome Project. We also assessed sex-by-age interactions to investigate sex differences in early postnatal brain development.ResultsOn average, males had significantly larger intracranial and total brain volumes, even after controlling for birth weight. After controlling for total brain volume, females showed significantly greater total cortical gray matter volumes, whilst males showed greater total white matter volumes. After controlling for total brain volume in regional comparisons, females had significantly increased white matter volumes in the corpus callosum and increased gray matter volumes in the bilateral parahippocampal gyri (posterior parts), left anterior cingulate gyrus, bilateral parietal lobes, and left caudate nucleus. Males had significantly increased gray matter volumes in the right medial and inferior temporal gyrus (posterior part) and right subthalamic nucleus. Effect sizes ranged from small for regional comparisons to large for global comparisons. Significant sex-by-age interactions were noted in the left anterior cingulate gyrus and left superior temporal gyrus (posterior parts).ConclusionsOur findings demonstrate that sex differences in brain structure are already present at birth and remain comparatively stable during early postnatal development, highlighting an important role of prenatal factors in shaping sex differences in the brain.

Brain morphometry and chronic inflammation in Bangladeshi children growing up in extreme poverty

Abstract Over three hundred million children live in environments of extreme poverty, and the biological and psychosocial hazards endemic to these environments often expose these children to infection, disease, and inflammatory responses. Chronic inflammation in early childhood has been associated with diminished cognitive outcomes, and despite this established relationship, the mechanisms explaining how inflammation affects brain development are not well known. Importantly, the prevalence of chronic inflammation in areas of extreme poverty raises the possibility that it may also serve as a mechanism explaining the known relationship between low socioeconomic status (SES) and altered brain development. To examine these potential pathways, seventy-nine children growing up in an extremely poor, urban area of Bangladesh underwent MRI scanning at 6 years of age. Structural brain images were submitted to Mindboggle software, a Docker-compliant and high-reproducibility tool for regional estimations of volume, surface area, cortical thickness, sulcal depth, and mean curvature. C-reactive protein was assayed at eight time points between infancy and 5 years of age, and the frequency with which children had elevated concentrations of inflammatory marker represented the measure of chronic inflammation. Childhood SES was measured with maternal education and income-to-needs (i.e., monthly household income divided by the number of household members). Chronic inflammation predicted volume in bilateral basal ganglia structures and mediated the link between maternal education and bilateral putamen volumes. These findings suggest that chronic inflammation is associated with brain morphometry in the basal ganglia, predominantly the putamen, and further offers inflammation as a potential mechanism linking SES to brain development.

Shedding Light on the Aftermath: Childhood Maltreatment's Role in Modifying the Association Between Recent Life Stress and Resting-State Network Connectivity.

Childhood maltreatment has been demonstrated to impact brain development. However, whether childhood maltreatment can influence the effects of recent stress on brain networks remains unclear. This study aimed to investigate whether childhood maltreatment moderates the longitudinal relationship between recent life stress and within- and between-network connectivity in key brain networks, including the anterior salience (ASN), central executive (CEN), default mode (DMN), and emotional regulation network (ERN). A cohort of 172 individuals from the Neuroscience in Psychiatry Network (NSPN) underwent MRI scans at two specific time points and undertook evaluations of childhood maltreatment and recent life stress. The results showed that childhood abuse moderated the association of recent life stress with the within-network connectivity of ASN and ERN but not DMN and CEN. Furthermore, recent life stress significantly interacted with childhood abuse to be associated with the between-network connectivity of ASN-DMN, ASN-CEN, ASN-ERN, DMN-ERN and CEN-ERN. Overall, among youth exposed to higher degrees of childhood abuse, greater recent life stress was longitudinally associated with increased network connectivity. Understanding these interactions can provide valuable insights for developing prevention strategies and interventions aimed at mitigating the lasting impact of childhood maltreatment on brain development and overall well-being.

Mechanism of cognitive processing for acupuncture action on generalized anxiety with naturally occurring consecutive partial sleep deprivation in early adulthood: a randomized controlled study and evaluation of event-related potentials

IntroductionGeneralized anxiety disorder (GAD) is a common mental disorder that often begins in adolescence or early adulthood and is characterized by widespread and persistent anxiety. Partial sleep deprivation (PSD) is an important risk factor for GAD development and a common comorbidity. Adolescence is a period of rapid brain and nervous system development, and during this time, the occurrence of GAD can lead to neurocognitive deficits, such as impaired attention, cognitive control, and attention bias, that significantly affect cognitive function. However, relatively little research has been conducted on GAD comorbid with PSD in early adulthood compared with other psychiatric disorders. Clinical studies have demonstrated the effectiveness of acupuncture in treating GAD and sleep disorders, but the mechanism of how acupuncture modulates neurocognitive processing in patients with GAD comorbid with PSD has not been clarified.Methods/designIn this randomized clinical trial, a total of 56 participants diagnosed with GAD comorbid with naturally occurring PSD and 28 healthy controls (HCs) will be recruited. The participants diagnosed with GAD comorbid with PSD will be randomly assigned to either the acupuncture group or the sham acupuncture group at a 1:1 ratio. The primary outcome measure is the Hamilton Anxiety Rating Scale (HAMA). Secondary outcome measures are the Sleep Deprivation Index (SDI), the Self-Assessment Scale for Anxiety (SAS), the Epworth Sleepiness Scale (ESS), and the State-Trait Anxiety Inventory (STAI). Additionally, three psychological paradigms (the attentional network test, psychomotor vigilance test, and emotional face Go/No-go) and event-related potential (ERP) data. Healthy volunteers will not undergo acupuncture but will instead participate in baseline assessments for the scales, mental paradigms, and ERP data. Acupuncture and sham acupuncture interventions will be conducted for 30 min, three times a week, over a 2-week period. Evaluations will be performed at zero weeks (baseline), 1 week, and 2 weeks, with the data enumerator, outcome assessor, and participant blinded to the treatment assignment.DiscussionThis study contributes to the exploration of the effects of acupuncture on improving anxiety symptoms and cognitive functions in individuals with comorbid GAD and PSD.Trial registrationClinicalTrials.gov, ChiCTR2400082221. Registered March 25, 2024.