International Journal of Developmental Neuroscience最新文献

{"title":"An Effective Autism Spectrum Disorder Detection Framework Using Adaptive Serial Hybrid Network With Self-Calibrated Feature Extraction on Brain MRI Images","authors":"Nandhini V,&nbsp;Ananthajothi K","doi":"10.1002/jdn.70187","DOIUrl":"10.1002/jdn.70187","url":null,"abstract":"<div>\u0000 \u0000 <p>Autism spectrum disorder (ASD) is a medical condition commonly categorized as a neurodevelopmental disorder. Patients with ASD are not limited to common symptoms, and it often requires long-term hospital visits and specialists for definitive evaluation. Research has highlighted the importance of early intervention and care for ASD patients, as it can benefit their lifestyle. Automated detection techniques through deep learners have shown great progress in detecting ASD, as they excel in handling highly complex features and functional activity patterns by evaluating magnetic resonance imaging (MRI). However, as the ASD-associated neuroimaging patterns are not explicitly shown in the MRI, several challenges remain in identifying the ASD related features from MRI evaluation. To overcome these challenges, an advanced deep learning framework has been developed for detecting ASD. In this proposed model, MRI scans are collected from accessible datasets and applied to the feature extraction process. Here, feature extraction was carried out with the support of the proposed Self-Calibrated Dense Convolution Vision Transformer (SC-DCVT). This proposed feature extraction model integrates dense connections and self-calibration mechanisms to capture rich, contextual features from the MRI images, improving the representation of complex patterns. Then, the extracted features are fed to the proposed Adaptive Serial Hybrid Autism Spectrum Disorder Detection Network (ASHASDDetN) model, which integrates two components, such as Residual-Temporal Convolutional Network (Res-TCN) with Dense Conditional Random Field (DCRF), to process ASD detection by capturing relevant features and ensuring its consistency. The reliability of the proposed ASHASDDetN model is enhanced by optimizing the parameters of Res-TCN and DCRF with the support of the Improved Position Updating Actor Optimization Algorithm (IPU-AOA) for the ASD detection task. The effectiveness of the proposed model is proven by conducting extensive experimentation among state-of-the-art techniques.</p>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"86 6","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149136560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of High-Phenolic Extra Virgin Olive Oil on Sensory Processing in Children With Autism Spectrum Disorder: A Pilot Study","authors":"Despoina Papastavridou,&nbsp;Eleni Baldimtsi,&nbsp;Aikaterini Katsiana,&nbsp;Magda Tsolaki","doi":"10.1002/jdn.70181","DOIUrl":"10.1002/jdn.70181","url":null,"abstract":"<p>No approved treatments currently exist for the core symptoms of autism spectrum disorder (ASD), prompting clinicians and families to seek alternative approaches, including dietary and nutritional interventions. The Mediterranean diet (MeDi), characterized by a high intake of antioxidant and anti-inflammatory components, is associated with improved health outcomes and reduced risk of chronic diseases. A key element of the MeDi is extra virgin olive oil (EVOO), which is rich in bioactive phenolics, including oleocanthal, oleuropein and hydroxytyrosol. Through its antioxidant and anti-inflammatory actions, EVOO may contribute to regulating pathological processes in both the central nervous system (CNS) and the gastrointestinal tract, offering a promising avenue for pharmacological and nutritional intervention in children with ASD. This pilot study investigated the effects of a three-month intervention combining the MeDi with EVOO supplementation on ASD symptoms. Ten children diagnosed with ASD aged 5.00–11.7 years, all boys, were recruited from Northern Greece. The changes in social interaction and communication were evaluated using standardized instruments: the Social Responsiveness Scale (SRS), Word Finding Vocabulary Test (WFVT), Autism Diagnostic Interview-Revised (ADI-R) and the Sensory Profile (SP). Paired-sample <i>t</i>-tests revealed significant improvements post-intervention in SRS (<i>p</i> = 0.034), ADI-R A (<i>p</i> = 0.008), WFVT (<i>p</i> = 0.020) and ADI-R B (<i>p</i> = 0.022) scores. These findings suggest that EVOO supplementation may reduce the severity of social deficits and enhance communication skills in children with ASD.</p>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"86 6","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13644697/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149127483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent Advances in Autism Spectrum Disorder Research on Epigenetics and Personalised Medicine","authors":"Rasa Khosrofar,&nbsp;Iman Morshedi,&nbsp;Mohammad Behzadpour,&nbsp;Narges Afzali,&nbsp;Reza Shah Hosseini,&nbsp;Alireza Aghili","doi":"10.1002/jdn.70184","DOIUrl":"10.1002/jdn.70184","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Autism spectrum disorder (ASD) is a multifaceted neurodevelopmental condition characterised by impairments in social interaction and communication, repetitive and restricted patterns of behaviour and atypical sensory processing. Although genetic susceptibility accounts for a substantial proportion of ASD risk, increasing evidence indicates that epigenetic modifications and environmental exposures play pivotal roles in disease development and progression.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Purpose</h3>\u0000 \u0000 <p>This review provides an updated overview of the current understanding of ASD pathogenesis, focusing on the interplay between epigenetic regulation, maternal health and the gut microbiome. It also highlights emerging diagnostic biomarkers and therapeutic strategies that have the potential to enhance early diagnosis and improve clinical management.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Main Findings</h3>\u0000 \u0000 <p>Recent studies indicate that maternal immune dysregulation, nutritional status, metabolic disorders and alterations in the maternal gut microbiota during pregnancy may contribute to ASD risk by inducing epigenetic changes and disrupting neurodevelopmental pathways. At the same time, novel pharmacological interventions aimed at alleviating behavioural symptoms and targeting epigenetic mechanisms are being actively explored. Advances in diagnostic technologies, including saliva-based microRNA profiling and epigenetic biomarkers, offer promising opportunities for earlier and more accurate ASD detection. Furthermore, genome-wide analyses and multi-omics approaches are facilitating the development of personalised diagnostic and therapeutic strategies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Despite considerable progress in elucidating the genetic and environmental factors associated with ASD, the disorder remains highly heterogeneous and biologically complex. Future research integrating epigenetic insights, microbiome investigations and precision medicine approaches will be crucial for uncovering the underlying molecular mechanisms and translating these discoveries into more effective diagnostic tools and targeted therapies.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"86 6","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149127472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Novel BORCS5 Loss-Of-Function Variant in a Patient With a Rare Neurodevelopmental Disorder","authors":"Arif Mahmood,&nbsp;Abid Ali Shah,&nbsp;Gohar Zaman,&nbsp;Shazra Masroof,&nbsp;Ahmed Waqas,&nbsp;Muhammad Umair","doi":"10.1002/jdn.70182","DOIUrl":"10.1002/jdn.70182","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The BORCS5 is an important and critical component of the BLOC-one-related complex (BORC), involved in kinesin-dependent anterograde lysosomal transport. Aberrations in the octameric protein complex encompass lethal neurological manifestations, such as arthrogryposis multiplex congenita, brain malformations and neuropathological evidence of diffuse neuroaxonal dystrophy. Loss-of-function variants in <i>BORCS5</i> are associated with extremely rapid and progressive neurodegeneration.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Herein, we present a family consisting of a proband with intellectual disability, microcephaly, developmental delay, facial dysmorphism, dystonia, focal/generalized seizures and speech delay. We performed whole-exome sequencing followed by Sanger sequencing for molecular diagnosis. Further, we performed 3D protein modelling for structural interpretation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Genetic analysis identified a novel stop-gain variant (NM_058169.6, c.262C&gt;T; NP_477517.1, p.(Gln88*)) in <i>BORCS5</i>, subsequently confirmed by Sanger sequencing. The variant is likely pathogenic (PVS1, PM2, PP3). Protein modelling of the BORCS5; p.(Gln88*) variant showed a distinct conformation compared with the wild-type BORCS5, suggesting a potential role for the unfolded protein response in the pathogenesis of BORCS5.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>In summary, our findings exemplify a novel stop-gain variant in <i>BORCS5</i> associated with diverse pathological manifestations, underscoring the importance of further exploring this gene in patients lacking identifiable disease-causing gene variants.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"86 6","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149109288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"REST in the Central Nervous System: Context-Dependent Regulation of Neuronal Homeostasis and Disease","authors":"Liebert Bernardes Carvalho,&nbsp;André Katayama Yamada,&nbsp;Lucas Alvarenga Furtado,&nbsp;Geórgia da Silva Feltran,&nbsp;Erick Ribeiro de Lima,&nbsp;Alexandre Paiva,&nbsp;Danielle Canineo,&nbsp;Maria Martha Bernardi,&nbsp;Célio Junior da Costa Fernandes,&nbsp;Rodrigo Augusto Foganholi da Silva","doi":"10.1002/jdn.70186","DOIUrl":"10.1002/jdn.70186","url":null,"abstract":"<div>\u0000 \u0000 <p>The RE1-silencing transcription factor (REST), also known as neuron-restrictive silencer factor (NRSF), is a zinc-finger domain-containing transcriptional regulator involved in coordinating gene expression programmes in the nervous system. Initially characterized as a repressor of neuronal genes in nonneuronal cells, REST also exerts context-dependent functions during neurodevelopment, neuronal maturation, homeostasis and brain ageing. Its activity involves the recruitment of multiple regulatory complexes, including Sin3A/HDACs and CoREST/LSD1, as well as interactions with mechanisms associated with DNA methylation and hydroxymethylation. REST also integrates regulatory networks involving noncoding RNAs. MicroRNAs such as miR-9, miR-124 and miR-132 participate in networks that interact with REST, contributing to the regulation of neuronal differentiation, maturation and function, whereas interactions with long noncoding RNAs remain less well characterized. Alterations in REST expression, subcellular localization or activity have been associated with various neurological and neurodegenerative conditions. In specific neuronal populations during ageing, nuclear REST has been associated with the regulation of genes involved in stress responses and neuronal resilience, whereas alterations in REST activity have been observed in diseases such as Alzheimer's and Huntington's disease. In addition, mechanistic evidence indicates that cellular metabolic state, particularly alterations in glycolysis and the NADH/NAD⁺ ratio, may influence REST-regulated pathways. In contrast, associations between REST and factors such as physical exercise and creatine availability remain predominantly indirect or hypothetical. In this review, we synthesize the evidence regarding the transcriptional and epigenetic regulatory mechanisms associated with REST, its interactions with noncoding RNA networks and its functions during neuronal development, homeostasis and ageing. We also discuss the interfaces between REST, metabolism and environmental factors, highlighting differences in the strength of the available evidence, current limitations and mechanistic gaps that warrant further investigation.</p>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"86 6","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149109229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plag1 Regulates Sensorimotor Modulation in Zebrafish","authors":"Jemma G. Gasperoni,&nbsp;Jarrad N. Fuller,&nbsp;April L. Lewis,&nbsp;Travis K. Johnson,&nbsp;Bert De Groef,&nbsp;Sebastian Dworkin","doi":"10.1002/jdn.70185","DOIUrl":"10.1002/jdn.70185","url":null,"abstract":"<p>The zinc finger transcription factor <i>PLAG1</i> has been implicated in multiple diverse cellular processes, yet its role in the onset of vertebrate neurodevelopment and behaviour remains largely unexplored. Notably, dysregulation of <i>PLAG1</i> has been associated with Silver–Russell syndrome (SRS) in humans, a growth disorder often presenting with neurodevelopmental delay and craniofacial abnormalities. Here, we investigate the function of <i>plag1</i> in zebrafish embryogenesis, focusing on behavioural phenotypes, neural development and craniofacial morphogenesis, as a potential novel model of SRS. Using antisense morpholino-mediated knockdown, we assessed the impact of <i>plag1</i> loss on brain architecture, motor neuron development, craniofacial patterning and stimulus-evoked behavioural responses. While <i>plag1</i>-deficient embryos displayed pronounced locomotor defects when housed in groups, these phenotypes were not recapitulated under isolated, individual tracking conditions, suggesting a role for <i>plag1</i> in modulating specific behavioural outputs. Morphological analyses revealed no overt disruptions to gross brain structure or primary motor neuron patterning. However, quantitation of craniofacial skeleton formation identified subtle abnormalities in jaw and cranial cartilage development, consistent with features observed in SRS. Furthermore, <i>plag1</i> morphants exhibited significantly altered responses to sensory stimuli, implicating <i>plag1</i> in the regulation of sensorimotor integration during early development. Collectively, these findings uncover a novel role for <i>plag1</i> in early neurobehavioural modulation and craniofacial patterning, phenocopying multiple features of SRS, and highlight the importance of environmental and social context in the phenotypic interpretation of neurodevelopmental gene function.</p>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"86 6","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13633108/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149109240","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MRI Characterization of Structural Brain Abnormalities in NGLY1 Deficiency.","authors":"Emily L Dennis, Lei Zhu, William F Mueller, Jennifer W Cook, Gracie Morrison, Matt Wilsey, Ryan Dant, Selina Dwight, Kevin J Lee","doi":"10.1002/jdn.70188","DOIUrl":"https://doi.org/10.1002/jdn.70188","url":null,"abstract":"<p><strong>Background and objectives: </strong>NGLY1 (N-Glycanase 1) deficiency is an ultrarare autosomal recessive disorder affecting ~165 patients worldwide, characterized by developmental delay, hyperkinetic movement disorders and shortened life expectancy. Despite its severe neurological manifestations, comprehensive neuroimaging characterization has been limited to case reports and small descriptive studies. Our objective was to investigate alterations in brain morphology in patients with NGLY1 deficiency and determine whether these metrics associate with clinical phenotypes.</p><p><strong>Methods: </strong>This case series analysed real-world MRI scans performed on 11 patients with molecularly diagnosed NGLY1 deficiency between 1999 and 2023 at sites across the globe. Ages ranged from 2 to 19 years at scan time (five female and six male). Cortical and subcortical morphology, including subcortical volume and cortical thickness, surface area, volume and curvature, was measured with three-dimensional T1-weighted magnetic resonance imaging (MRI) scans. Z scores were calculated using normative models from CentileBrain for patients > 3 years old or custom models for patients < 3 years old. Clinical phenotypes were matched to Human Phenotype Ontology codes.</p><p><strong>Results: </strong>Sixteen scans from 11 patients met quality criteria for analysis. Both age groups (under and over 3 years old) showed significantly reduced subcortical volumes, particularly in bilateral thalamus and putamen. Younger patients demonstrated widespread reductions in cortical surface area, volume and curvature, indicating altered gyrification patterns. Older patients showed thinner dorsal and thicker ventral cortical regions with limited surface area reductions. Thalamic volume reduction in older patients correlated with gait disturbance, dysphagia and EEG abnormalities, with additional cortical associations with sleep and hearing abnormalities. Seizure presence in younger patients correlated with altered cortical thickness, surface area and curvature patterns.</p><p><strong>Discussion: </strong>NGLY1 deficiency is associated with pervasive alterations in brain development affecting both subcortical and cortical morphology. Age-dependent patterns of cortical alterations indicate disrupted neurodevelopmental trajectories that may reflect impaired neuronal migration and/or altered synaptic pruning. Correlations with clinical variables suggest that these measures may serve as useful biomarkers for tracking disease progression and/or treatment efficacy. These findings provide a comprehensive neuroimaging characterization of NGLY1 Deficiency and establish a foundation for understanding brain structure-function relationships in this ultrarare disorder.</p>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"86 6","pages":"e70188"},"PeriodicalIF":1.4,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149223965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic Potential of Pioglitazone in a Propionic Acid-Induced Rat Model of Autism Spectrum Disorder: The Role of the SIRT1/PPAR-γ Axis","authors":"Arife Erdoğan,&nbsp;Mümin Alper Erdoğan,&nbsp;Yiğit Uyanıkgil,&nbsp;Oytun Erbaş","doi":"10.1002/jdn.70180","DOIUrl":"10.1002/jdn.70180","url":null,"abstract":"<div>\u0000 \u0000 <p>Autism spectrum disorder (ASD) is a complex neurodevelopmental condition characterized by social communication deficits and repetitive behaviours. Emerging evidence highlights neuroinflammation, oxidative stress and mitochondrial dysfunction in its pathogenesis. Propionic acid (PPA), an enteric short-chain fatty acid, is frequently utilized to replicate ASD-like phenotypes in rodents. This study investigated the therapeutic efficacy of pioglitazone, a peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist known for its neuroprotective and anti-inflammatory properties, in a PPA-induced rat model of ASD. Thirty male Wistar rats were randomly assigned to control, PPA + saline or PPA + pioglitazone (15 mg/kg/day, orally) groups. Neurobehavioural profiling utilized the sociability, open-field and passive avoidance learning tests. Furthermore, cerebral tissues were analysed for tumour necrosis factor-alpha (TNF-α), brain-derived neurotrophic factor (BDNF), sirtuin-1 (SIRT1), galectin-3 and malondialdehyde (MDA), alongside comprehensive histopathological evaluations of the hippocampus and cerebellum. Pioglitazone significantly improved social interaction, associative memory retention and spontaneous locomotor activity. Biochemically, the treatment significantly suppressed inflammatory and oxidative stress markers (TNF-α, galectin-3 and MDA) while increasing cerebral BDNF and SIRT1 levels. Histological assessments confirmed these neuroprotective benefits, demonstrating preserved neuronal architecture and decreased glial fibrillary acidic protein (GFAP) immunoreactivity, indicative of reduced reactive astrogliosis. These findings indicate that pioglitazone ameliorates behavioural, biochemical and histopathological alterations in the PPA-induced rat model of ASD. The concurrent restoration of cerebral SIRT1 levels suggests that SIRT1-related signalling may contribute to the observed neuroprotective effects.</p>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"86 6","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149069615","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal Immune Activation and Intermittent Maternal Hypoxic Stress Exacerbate Ischaemic Stroke in Adult Rats: A Two-Hit Biochemical Hypothesis Study Across Developmental Stages","authors":"Faith B. Friday,&nbsp;Benneth Ben-Azu,&nbsp;Prosper Iwhiwhu,&nbsp;Joseph Chimezie,&nbsp;Esther O. Ozah,&nbsp;Saviour G. Usin,&nbsp;Bienose S. Chijioke,&nbsp;Daniel T. Esuku,&nbsp;Ayereoghene S. Moses,&nbsp;Emmanuel O. Chidebe,&nbsp;Jackson E. Onuelu,&nbsp;Samuel K. D. Bamitale,&nbsp;Isaac T. Henneh","doi":"10.1002/jdn.70179","DOIUrl":"10.1002/jdn.70179","url":null,"abstract":"<div>\u0000 \u0000 <p>The developmental origins of health and disease hypothesis states that prenatal immune activation (PIA) and hypoxic stress contribute to long-term susceptibility to neurological disorders, including ischaemic stroke. However, an understanding of the interplay between PIA and intermittent maternal hypoxic stress (IMHS) in animal models of ischaemic stroke vulnerability remains unknown. We developed an experimental approach to examine how PIA and IMHS together affect neurological and biochemical outcomes in a rat model of ischaemic stroke caused by bilateral common carotid artery occlusion/reperfusion (BCCAO/R). PIA was induced with lipopolysaccharide (0.1 mg/kg, ip) injection at gestational day (GD) 15, followed by IMHS exposure from GD 17 to delivery. Male and female offspring of dams from different groups were divided into the following cohorts: sham control, BCCAO/R (from naïve rats), LPS-exposed, hypoxia-exposed and LPS + hypoxia coexposed (<i>n</i> = 10 per sex). After monitoring behavioural, neurological phenotypes during infancy, adolescence and adulthood using various neurological test tools, we conducted BCCAO/R-induced cerebral hypoperfusion at postnatal day (PND) 90 in adult offspring (Groups 2–5) to assess ischaemic stroke vulnerability. Afterwards, neurological deficits and behavioural tests were re-conducted at 1 and 5 h postsurgery. Behavioural characterisation across infancy (PNDs 25–30), adolescence (PNDs 35–40) and adulthood (PNDs 85–88) served as developmental phenotyping of the prenatal stressor model and was not performed in the context of stroke induction. The prefrontal cortex and striatum were analysed for oxidative markers, molybdoenzymes, cholinergic function and inflammatory markers (myeloperoxidase, interleukin-1β and interleukin-4), which are implicated in the disease. Combined PIA + IMHS significantly intensified post-reperfusion neurological and motor impairments, elevated lipid peroxidation and nitrergic stress and suppressed antioxidant defences, notably in females. These prenatal stressors shifted cytokine profiles toward inflammation and increased myeloperoxidase activity. Females showed higher striatal IL-1β responses and cortical cholinergic dysfunction, worsening ischaemic vulnerability through oxidative–inflammatory mechanisms.</p>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"86 6","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149024852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Psychometric Evaluation of the Turkish Mind Excessively Wandering Scale in Adolescents With ADHD: Exploratory Findings on Age-Related Differences in Excessive Mind Wandering","authors":"Hasan Ali Güler,&nbsp;Binaz Bozkur,&nbsp;Ülkü Hüma Akbulut,&nbsp;Mustafa Esad Tezcan,&nbsp;Ali Kandeğer","doi":"10.1002/jdn.70175","DOIUrl":"https://doi.org/10.1002/jdn.70175","url":null,"abstract":"<div>\u0000 \u0000 <p>This study examined the psychometric properties of the Turkish version of the Mind Excessively Wandering Scale (MEWS) in adolescents and investigated age-related differences in excessive mind wandering (EMW) among adolescents with ADHD. The sample included 156 adolescents (80 with ADHD, 76 controls; mean age = 15.08 ± 1.85 years). ADHD diagnoses were established using a semi-structured clinical interview. Participants completed the MEWS, DERS-16 and S-UPPS-P. Confirmatory factor analysis (CFA), reliability analyses, group comparisons and regression analyses were conducted. The MEWS showed a unidimensional structure with acceptable model fit and high internal consistency (<i>α</i> = 0.93). EMW was significantly higher in the ADHD group than in controls. EMW was strongly associated with emotion regulation difficulties and moderately associated with impulsivity and ADHD symptoms. A significant age × group interaction was observed, indicating that the relationship between age and EMW differed across diagnostic groups. Older adolescents with ADHD tended to report higher EMW scores than younger adolescents with ADHD, whereas no comparable age-related pattern was observed in the control group. The original 12-item Turkish MEWS demonstrated good psychometric performance in the present adolescent sample. The present findings suggest that EMW may show age-related differences among adolescents with ADHD. Whether these differences reflect developmental changes across adolescence requires confirmation in longitudinal studies.</p>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"86 6","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148962556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}