International Journal of Developmental Neuroscience最新文献

{"title":"Correction to ‘Therapeutic Effect of Perinatal Exogenous Melatonin on Behavioral and Histopathological Changes and Antioxidative Enzymes in Neonate Mouse Model of Cortical Malformation’","authors":"","doi":"10.1002/jdn.70035","DOIUrl":"https://doi.org/10.1002/jdn.70035","url":null,"abstract":"<p>\u0000 <span>Azizi, M.</span>, <span>Pasbakhsh, P.</span>, <span>Nadji, S.A.</span>, <span>Pourabdollah, M.</span>, <span>Mokhtari, T.</span>, <span>Sadr, M.</span>, <span>Omidi, N.</span>, <span>Kashani, I.R.</span>, and <span>Zendehdel, A.</span> <span>2018</span>. “ <span>Therapeutic Effect of Perinatal Exogenous Melatonin on Behavioral and Histopathological Changes and Antioxidative Enzymes in Neonate Mouse Model of Cortical Malformation</span>.” <i>International Journal of Developmental Neuroscience</i> <span>68</span>: <span>1</span>–<span>9</span>. https://doi.org/10.1016/j.ijdevneu.2018.03.008.\u0000 </p><p>In Figure 2A, the image for the control (Co) group was mistakenly replaced with the MAM + MEL2 group image, which is inconsistent with the statistical results in Figure 7. Additionally, the magnified inset in the MAM group panel was incorrectly sourced from the main figure, misrepresenting the magnified region.</p><p>We apologize for this error.</p>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"85 5","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jdn.70035","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144869721","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":"Long-Term Clinical Characterization of ENTPD1-Related Spastic Paraplegia: A Novel Variant and Comprehensive Literature Review","authors":"Dilsu Dicle Erkan,&nbsp;Oğuz Lafcı,&nbsp;Ülkühan Öztoprak,&nbsp;Göknur Haliloğlu,&nbsp;Naz Güleray","doi":"10.1002/jdn.70046","DOIUrl":"https://doi.org/10.1002/jdn.70046","url":null,"abstract":"<div>\u0000 \u0000 <p>Hereditary spastic paraplegia (HSP) represents a genetically heterogeneous group of neurodegenerative disorders characterized by progressive axonal degeneration of corticospinal upper motor neurons, leading to lower limb-predominant spasticity and weakness. To date, 83 HSP subtypes have been reported, exhibiting either pure or complicated phenotypes. Among these, spastic paraplegia type 64 (SPG64) is an ultra-rare form of complicated HSP caused by biallelic variants in <i>ENTPD1</i>, which encodes an ectonucleotidase involved in purine metabolism. In this study, we report a proband presenting with neurodevelopmental regression, dysmorphic features and sensorimotor polyneuropathy, followed comprehensively for 6 years. Genetic analysis identified a novel homozygous NM_001776:c.1174C&gt;T;p.Gln392Ter variant in <i>ENTPD1</i>. A literature review reveals that 39 individuals with SPG64 have been reported, with clinical manifestations including cognitive decline (38/39), speech abnormalities (30/39) and brain malformations (16/31). However, aspects of the full phenotypic spectrum remain to be fully characterized. Notably, this case represents the first documented patient with long-term follow-up, providing valuable clinical insights into disease progression over time. Neuroimaging in the proband demonstrated the involvement of the posterior limb of the internal capsule and the ‘ear of the lynx’ sign, which was not previously reported in SPG64. Furthermore, the presence of sensorimotor polyneuropathy supports that neuropathy may be a previously unappreciated component of SPG64. Our findings highlight the importance of deep phenotyping and long-term follow-up in fully understanding the nature of this unique HSP subtype.</p>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"85 5","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144869571","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":"Whole Brain Spectral Power Differences During Infancy Following Antenatal SARS-CoV-2 and Zika Virus Exposure: Findings From Cohorts in Boston, Massachusetts and San Juan, Puerto Rico","authors":"Viviane Valdes,&nbsp;Dashiell D. Sacks,&nbsp;Jennifer Near,&nbsp;Adriana S. Méndez Leal,&nbsp;Andrea G. Edlow,&nbsp;Carmen D. Zorrilla,&nbsp;Charles A. Nelson","doi":"10.1002/jdn.70047","DOIUrl":"https://doi.org/10.1002/jdn.70047","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Viral exposure during pregnancy is associated with adverse outcomes in offspring. Given the increasing frequency of viral outbreaks both locally and globally, the current study sought to examine the impact of antenatal exposure to Zika virus (ZIKV) and SARS-CoV-2 on infant neurophysiological development during the first year of life.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Families were recruited from two cohorts, one in San Juan, Puerto Rico (ZIKV) and one in Boston, Massachusetts (SARS-CoV-2). For the ZIKV cohort, infants were assessed cross-sectionally between 3 to 12 months of age. For SARS-CoV-2, infants were assessed longitudinally at 3, 6, 9 and 12 months. Electroencephalography (EEG) was used to compare absolute power during a resting state task across the whole brain (by spectral band) between infants with antenatal viral exposure and nonexposed infants. Data were analysed using generalized linear models (GLMs) and multilevel mixed effects models.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In the ZIKV cohort, age-by-exposure interactions were observed for delta (<i>p</i> = 0.027) and theta power (<i>p</i> = 0.009), where exposed infants demonstrated decreasing power with age, while nonexposed infants demonstrated increasing power with age from 3 to 12 months. In the SARS-CoV-2 cohort, antenatally exposed children had lower levels of beta (<i>p</i> = 0.022) and gamma power (<i>p</i> = 0.044) overall from 3 to 12 months. Significant recovery was observed in trajectories for beta power by 12 months.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>ZIKV exposure during pregnancy was associated with reductions in low-frequency EEG power, which may be indicative of disruptions in early brain maturation. SARS-CoV-2 exposure was associated with reductions in higher-frequency power, suggesting potential impairments on sensorimotor and cognitive integration. Increases in beta power by 12 months in the SARS-CoV-2 cohort indicate some recovery, although potential compounding and sleeper effects from early disruptions are possible.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"85 5","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144869572","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":"Quality of Life and Anxiety of Adolescents With Cancer and Their Parents: Neurodevelopmental Implications in Adolescence","authors":"Kalliopi Megari,&nbsp;Dimitra V. Katsarou,&nbsp;Evangelos Mantsos,&nbsp;Vasiliki Miliadi,&nbsp;Elina Kosmidou,&nbsp;Agathi Argyriadi,&nbsp;Soultana Papadopoulou,&nbsp;Alexandros Argyriadis,&nbsp;Eugenia. I. Toki,&nbsp;Maria Sofologi","doi":"10.1002/jdn.70040","DOIUrl":"https://doi.org/10.1002/jdn.70040","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Cancer is one of the most lethal chronic diseases, which has been the reason for the majority of losses of lives globally. Adolescents with cancer experience a lower quality of life compared to both their healthy peers and adult patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In the present study, 237 adolescents and 460 parents were evaluated with measures of quality of life and anxiety.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>All patients showed lower performance on QoL and increased performance on anxiety measures. Regarding parents' QoL, although parents of all groups had low performance on all measures, parents of adolescents with leukaemia experience poor quality of life and increased levels of anxiety.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Adolescents and young adults with cancer are going through a turbulent period of their lives, not only due to their diagnosis and treatment process but also due to the physical and psychosocial changes and neurodevelopmental consequences of paediatric cancer and its treatment in adolescence.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"85 5","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144832438","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":"Reelin/Disabled-1 Signalling Contributes to Functional Recovery on Zebrafish After Spinal Cord Injury","authors":"Rong Li,&nbsp;Sudhanshu Sahu","doi":"10.1002/jdn.70045","DOIUrl":"https://doi.org/10.1002/jdn.70045","url":null,"abstract":"<div>\u0000 \u0000 <p>Reelin, an extracellular matrix glycoprotein, plays important roles in neural development. Mutation-induced loss of its functions in mammals leads to severe disorders associated with impaired motor coordination, tremors and ataxia. Little is known about Reelin's role in functional recovery after central nervous system injury. We determined the effect of knock-down of Reelin and its downstream signal-transducing molecule Disabled-1 (Dab-1) on functional recovery after spinal cord injury in larval zebrafish. Larvae deficient in Reelin and Dab-1 were generated by application of two non-overlapping antisense morpholinos for each molecule. Individual knock-down of Reelin and Dab-1 expression impaired locomotor recovery after injury, inhibited remyelination of regrown axons and reduced numbers of motor neurons caudal to the lesion site. These results indicate that the Reelin/Dab-1 signalling pathway is involved in axon regeneration after injury of a paradigmatic vertebrate in the central nervous system.</p>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"85 5","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144832476","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":"PGAP1-Related Encephalopathy in an Infant With Neurodevelopmental Delay: Novel Variant and Review of Literature","authors":"Savas Baris,&nbsp;Cuneyd Yavas","doi":"10.1002/jdn.70044","DOIUrl":"https://doi.org/10.1002/jdn.70044","url":null,"abstract":"<p>Spastic paraplegia-67, caused by a defect in glycosylphosphatidylinositol (GPI) biosynthesis, is an autosomal recessive neurodevelopmental disorder. It is characterized by dysmorphic features, spasticity, brain abnormalities, hypotonia, impaired intellectual development and speech difficulties. A 9-month-old girl was admitted to our clinic with a neurodevelopmental disorder, hepatomegaly, occasional vomiting, spasticity and hypotonicity. Whole exome sequencing (WES) was planned in the patient who had microcephaly, dysmorphic facial appearance, short and blunt fingers, a wide mouth, lacking physical sensation, dyskinetic movements, agenesis of the corpus callosum and cerebellar hypoplasia on MRI. In our study, we used whole-exome sequencing, family segregation and bioinformatics to identify a homozygous 3 bp duplication in the GPI remodelling gene <i>PGAP1</i> (c.1226_1229dup p.(Val411Argfs*3) [NM_024989.4]) in a female patient with a neurodevelopmental disorder, encephalopathy and nonspecific autosomal recessive forms of intellectual disability (ARID). At least 26 genes are involved in the biosynthesis and remodelling of GPI junctions. Hypomorphic coding variants in seven of these genes have been reported to cause reduced expression of GPI-associated proteins (GPI-APs) on the cell surface and ARID. <i>PGAP1</i> gene variants are important in understanding GPI biosynthesis defects, which can lead to severe neurodevelopmental disorders like spastic paraplegia-67. The identified homozygous variant (c.1226_1229dup) further expands the genetic spectrum of GPI-related disorders and underscores the role of WES in diagnosing rare encephalopathies with dysmorphic features.</p>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"85 5","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jdn.70044","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144811176","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":"Rapid Electroclinical Evolution in HECW2-Related Developmental and Epileptic Encephalopathy: Report of a Likely Splicing Variant With Familial Transmission","authors":"Sergio Melgarejo,&nbsp;Gabriela Reyes Valenzuela,&nbsp;Matías Juanes,&nbsp;Maria Sol Touzon,&nbsp;Carol Suyo,&nbsp;Cristina Alonso,&nbsp;Amin Gauto,&nbsp;Juan Pablo Princich,&nbsp;Mariana Loos,&nbsp;Roxana Obregón,&nbsp;Ana Pérsico,&nbsp;Roberto Caraballo","doi":"10.1002/jdn.70041","DOIUrl":"https://doi.org/10.1002/jdn.70041","url":null,"abstract":"<div>\u0000 \u0000 <p>The <i>HECW2</i> gene, essential for neurodevelopment, plays a critical role in maintaining cellular homeostasis and regulating key pathways in the nervous system. Deleterious variants in the <i>HECW2</i> gene have been associated with developmental delay, intellectual disability, hypotonia and epilepsy, as well as dysmorphic features. We present the case of an infant with a novel variant in <i>HECW2</i> with an unusual clinical presentation and a progressive disease course, showing three successive electroclinical patterns, consisting of burst suppression characteristic of early infantile developmental and epileptic encephalopathy, subcontinuous myoclonic seizures and infantile epileptic spasms syndrome without hypsarrhythmia, occurring over a short period of time. This case expands the clinical spectrum associated with this gene and highlights the intrafamilial phenotypic variability. It also underscores the importance of personalized therapeutic strategies, as demonstrated by the use of perampanel in this patient. These findings emphasize the need to include <i>HECW2</i> as a possible aetiology in the diagnostic evaluation of developmental and epileptic encephalopathies.</p>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"85 5","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144782441","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":"Moyamoya Syndrome, Epilepsy and Hydrocephalus in Neurofibromatosis Type 1","authors":"Fen Zhao,&nbsp;Xizan Yue,&nbsp;Guangyu Wang,&nbsp;Hongwei Zhang","doi":"10.1002/jdn.70038","DOIUrl":"https://doi.org/10.1002/jdn.70038","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Neurofibromatosis type 1 (NF1) is an autosomal dominant neurocutaneous syndrome. NF1-related vasculopathy represents a clinically significant yet underrecognized complication. Moyamoya syndrome, a rare cerebrovascular manifestation of NF1, has been rarely reported in the paediatric population. Epilepsy and hydrocephalus are also uncommon neurological manifestations of NF1. However, the co-occurrence of the above three symptoms in NF1 cases is rarely found.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Here, we report a 2-year-old boy with moyamoya syndrome, epilepsy and hydrocephalus caused by de novo <i>NF1</i> pathogenetic variants.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>He experienced a 1-week history of paroxysmal hands weakness and frequent seizures. Physical examination showed macrocephaly (head circumference was 52 cm), reduced distal muscle strength in both upper limbs (grade III) and the presence of 6 or more café-au-lait macules (CALMs). Brain magnetic resonance imaging (MRI) showed moyamoya syndrome and hydrocephalus. Electroencephalographic (EEG) monitored two episodes of electrical persistent seizures and one focal motor seizure. Trio whole exome sequencing (Trio-WES) demonstrated a de novo and heterozygous <i>NF1</i> missense mutation (c.5488C &gt; G, p. Arg1830Gly). The final diagnoses were ‘neurofibromatosis type 1, moyamoya syndrome, epilepsy, and hydrocephalus’. Following surgical intervention and treatment with levetiracetam, the patient achieved normal muscle strength and was seizure-free.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>When articles about complications of NF1 are placed in a separate category, little is written about NF-1-related moyamoya syndrome, hydrocephalus and epilepsy simultaneously. This report describes a case of NF1 with moyamoya syndrome combined with hydrocephalus and epilepsy, which could enhance clinicians' understanding of the neurological manifestations of NF1 and provide reference value for clinical practice.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"85 5","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jdn.70038","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144767812","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":"Rare Presentations of GLUT1 Deficiency Syndrome: Rare Variants With Cortical Dysplasia in Two Unrelated Families","authors":"Hilal Aydin,&nbsp;Zeynep Esener,&nbsp;Hilmi Bolat,&nbsp;Adil Aytaç","doi":"10.1002/jdn.70039","DOIUrl":"https://doi.org/10.1002/jdn.70039","url":null,"abstract":"<div>\u0000 \u0000 <p>Glucose transporter type 1 deficiency syndrome (GLUT1DS) affects all age groups, from infants to adolescents, and involves age-specific symptoms. Nonclassic GLUT1 DS is observed in 10% of cases, in which seizures are not observed, and the condition involves a milder accompanying phenotype and paroxysmal dyskinesias. Cranial imaging findings in cases of GLUT1 DS are variable. The purpose of this report is to describe rare genetic variants in two cases of GLUT1 DS with cortical dysplasia detected at magnetic resonance imaging (MRI) and exhibiting differing clinical presentations and to discuss the relationship between them. Two cases presenting to the Balıkesir University Medical Faculty paediatric neurology clinic, Türkiye, between 01.08.2019 and 01.12.2024 due to seizures and inability to speak/numbness in the hands and arms, diagnosed as GLUT1 DS, and with cortical dysplasia, were included. The patients' files, MRI and physical examination findings and family pedigrees were evaluated. We detected two different pathogenic and likely pathogenic variants in <i>SLC2A1</i> (NM_006516.3) in patients from unrelated families. Patient 1 exhibited a heterozygous c. 1208C &gt; T variant and patient 2 a heterozygous likely c. 278G &gt; A variant. In conclusion, the careful evaluation of patients with structural brain damage and determination of the molecular aetiology of underlying inherited metabolic diseases are highly important in terms of the provision of treatment, prognosis, and genetic counselling. Although cortical malformations have been reported in patients with GLUT1 DS, the mechanism involved remains unclear, and this report highlights the potential relationship between cortical dysplasia and specific genotypes in GLUT1 DS. Further prospective observational and functional studies involving larger numbers of cases and centres are now needed.</p>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"85 5","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144767317","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":"Associations Between Experience of Typical Variations in Stressors and Hippocampal Structure and Functional Connectivity in Childhood","authors":"Morgan Botdorf,&nbsp;Zehua Cui,&nbsp;Tracy Riggins","doi":"10.1002/jdn.70037","DOIUrl":"https://doi.org/10.1002/jdn.70037","url":null,"abstract":"<p>Abuse and maltreatment have been associated with negative effects on the developing brain through the hypothalamic–pituitary–adrenal (HPA) axis, the body's central stress response system. Theoretically, similar pathophysiology occurs when children experience more moderate forms of stress (i.e., changing schools); however, evidence for this association is lacking. Therefore, the current study explored the effects of typical variations in stressful life events on the development of the hippocampus, a brain region susceptible to stress. Data from a 3-year accelerated longitudinal sample of 4- and 6-year-old children were used to assess the links between stressful events and the development of hippocampal subfield volumes (<i>N</i>_total = 90) and functional connectivity (<i>N</i>_total = 83). In the 4-year-old cohort, stressful experiences were related to an overall slower growth in CA1 and subiculum volume from age 5 to 6. In the 6-year-old cohort, stressful experiences were related to smaller CA2–4/DG volume at age 6 and an overall faster decrease in subiculum volume from age 6 to 7. Small effects were observed regarding the relations between stress and hippocampal functional connectivity; however, they did not survive multiple comparisons. Results from analyses comparing cohorts showed that the relations between stressful events and CA2–4/DG volume and change in subiculum volume significantly differed between the younger and older cohorts. Overall, these findings demonstrate the links between typical variations in stress and hippocampal development and highlight the region- and age-specific nature of the effects of stress. Together, this work emphasizes the importance of understanding how brain development may be influenced by stress in all forms, as stress-related alterations in hippocampal development have been linked to variations in cognitive processes (e.g., memory) and risk for psychopathology (e.g., major depressive disorder).</p>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"85 5","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jdn.70037","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144767585","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}