International Journal of Developmental Neuroscience最新文献

{"title":"Amelioration of propionic acid-induced autism-like behaviors in rats by fenofibrate: A focus on reduction of brain galectin-3 levels","authors":"Mumin Alper Erdogan,&nbsp;Mine Ceren Akbulut,&nbsp;İlknur Altuntaş,&nbsp;Canberk Tomruk,&nbsp;Yiğit Uyanıkgil,&nbsp;Oytun Erbaş","doi":"10.1002/jdn.10393","DOIUrl":"10.1002/jdn.10393","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social interactions and repetitive behaviors. This study examines the effects of fenofibrate on a propionic acid (PPA)-induced rat model of ASD, focusing on behavioral changes, inflammatory markers, and histological findings.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>Thirty male Wistar rats were divided into three groups: a control group, a group receiving PPA and saline, and a group treated with PPA and fenofibrate for 15 days. Behavioral assessments, including the three-chamber sociability test, open-field test, and passive avoidance learning, were conducted. Biochemical analyses measured TNF-α, NGF, IL-17, IL-2, and galectin-3 levels in brain tissues. Histological evaluations focused on Purkinje neuron counts in the cerebellum and neuronal changes in the CA1 and CA3 regions of the hippocampus, along with glial fibrillary acidic protein (GFAP) levels.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Fenofibrate treatment significantly improved behavioral outcomes, reducing autism-like behaviors compared to the PPA/saline group. Biochemically, the PPA/saline group showed elevated levels of malondialdehyde, TNF-α, IL-2, IL-17, and galectin-3, which were reduced following fenofibrate treatment. Histologically, the PPA/saline group exhibited fewer, dysmorphic Purkinje neurons and increased glial activity in the CA1 region, both of which were ameliorated by fenofibrate treatment.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Fenofibrate shows promise in mitigating autism-like behaviors in a rat model of ASD, likely due to its antioxidative and neuroprotective properties, which contribute to preserving neuronal integrity and reducing inflammation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"84 8","pages":"977-990"},"PeriodicalIF":1.7,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619650","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 effects of pentoxifylline in propionic acid-induced autism symptoms in rat models: A behavioral, biochemical, and histopathological study","authors":"Mümin Alper Erdoğan,&nbsp;Kerem Can Tunç,&nbsp;Ali İmran Daştan,&nbsp;Canberk Tomruk,&nbsp;Yiğit Uyanıkgil,&nbsp;Oytun Erbaş","doi":"10.1002/jdn.10394","DOIUrl":"10.1002/jdn.10394","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>The role of propionic acid (PPA) in eliciting behaviors analogous to autism in rat models is a documented phenomenon. This study examines the therapeutic implications of pentoxifylline—an agent traditionally used for peripheral vascular diseases—on these autism-like behaviors by modulating brain proteins and reducing pro-inflammatory cytokines like tumor necrosis factor-α (TNF-α) in a rat model.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This research involved 30 male <i>Wistar albino</i> rats, which were divided into three distinct groups: a baseline control set, a PPA-treated cluster receiving a 250 mg/kg/day dose of PPA via intraperitoneal injection for a span of five days followed by saline orally, and a PPA group administered an oral dose of pentoxifylline at 300 mg/kg/day over 15 days. Subsequent to the treatment phase, euthanasia was carried out for the extraction of brain and blood samples, which were then analyzed for histopathological and biochemical markers.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The pentoxifylline-treated subjects demonstrated a significant mitigation in the manifestation of autistic-like behaviors, as assessed through a triad of social interaction tests. A noteworthy decline in TNF-α levels was observed, alongside a significant rise in the concentration of adenosine triphosphate and nerve growth factor in brain tissue (p &lt; 0.05). Histopathological analysis underscored a reduction in oxidative stress and a significant preservation of neuronal cell types, specifically pyramidal neurons in the hippocampal CA1 and CA3 regions and Purkinje cells in the cerebellum (p &lt; 0.001).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Pentoxifylline treatment has been found to effectively reduce the behavioral symptoms associated with autism, as well as biochemical and histopathological disruptions induced by PPA in rat models, highlighting its potential as a neurotherapeutic agent.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"84 8","pages":"991-1005"},"PeriodicalIF":1.7,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619688","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":"Exposure to Sunset Yellow FCF since post-weaning causes hippocampal structural changes and memory impairment in the adult rat: The neuroprotective effects of Coenzyme Q10","authors":"Seyed Reza Mousavi,&nbsp;Maryam Shadravanan,&nbsp;Majid Reza Farrokhi,&nbsp;Fatemeh Karimi,&nbsp;Narges Karbalaei,&nbsp;Melika Arzhang zadeh,&nbsp;Maryam Naseh","doi":"10.1002/jdn.10385","DOIUrl":"10.1002/jdn.10385","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>This study aimed to investigate whether exposure to Sunset Yellow FCF (SY) since post-weaning can lead to hippocampal structural changes and memory impairment in adult rat and whether the Coenzyme Q10 (CoQ10) can protect against these adverse effects.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The weanling rats were randomly divided into six groups and were treated daily by oral gavage for 6 weeks, as follows: (I) control group, administered distilled water (0.3 mL/100 g/day); (II) CoQ10 group, received 10 mg/kg/day CoQ10; (III) low SY group, received 2.5 mg/kg/day SY; (IV) high SY group, received 70 mg/kg/day SY; (V) low SY + CoQ10 group; and (VI) high SY + CoQ10 group. At the end of the sixth week, the novel object recognition (NOR) test was conducted to evaluate memory. Then, after sacrificing animals, the cerebral hemispheres were removed for stereological study and evaluation of MDA levels.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The low and high doses of SY led to significant neuronal loss and a decrease in the volume of the hippocampus (CA1 and DG subregions), as well as increased the MDA level, which was associated with short- and long-term memory impairment. Although, administration of CoQ10 prevented the hippocampal neural loss and volume, and caused a reduction in MDA and improved memory in the low and high SY groups.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>It seems that CoQ10 could prevent the neuronal loss and hippocampal atrophy caused by post-weaning exposure to SY through preventing oxidative stress, ultimately improving memory impairment in rats.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"84 8","pages":"924-933"},"PeriodicalIF":1.7,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619678","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":"GABA in early brain development: A dual role review","authors":"Xiaoyu Ji,&nbsp;Shuzhen Liu,&nbsp;Shiyong Li,&nbsp;Xing Li,&nbsp;Ailin Luo,&nbsp;Xue Zhang,&nbsp;Yilin Zhao","doi":"10.1002/jdn.10387","DOIUrl":"10.1002/jdn.10387","url":null,"abstract":"<p>This comprehensive review examines the multifaceted roles of gamma-aminobutyric acid (GABA) in early brain development. GABA, traditionally recognized for its inhibitory functions in the mature brain, also exhibits excitatory effects during early neural development. This article explores the mechanisms behind GABA's dual roles, detailing its impact on the properties of the immature brain, the mechanisms of GABA-mediated excitation, the role of GABA-mediated presynaptic inhibition, the trophic actions of GABA during early development, GABA regulation of neurite growth and GABA-mediated cell differentiation in the immature brain. Emphasizing recent research findings, the review highlights the significance of GABAergic signalling in shaping the developing brain and its potential implications for understanding neurodevelopmental disorders.</p>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"84 8","pages":"843-856"},"PeriodicalIF":1.7,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142582892","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 MAOA gene variant: Brunner syndrome, a rare syndrome, is associated with a wide range of psychiatric symptoms","authors":"Gül Ünsel-Bolat,&nbsp;Sıla Turan,&nbsp;Hilmi Bolat","doi":"10.1002/jdn.10390","DOIUrl":"10.1002/jdn.10390","url":null,"abstract":"<p>Brunner syndrome is a rare genetic disorder that associated with mutations in the <i>MAOA</i> gene. It has been linked to a number of psychiatric disorders. We present detailed information on psychiatric evaluation of a case carrying a novel <i>MAOA</i> gene variant of p.(Thr408Met). The patient was referred to our clinic with a history of attention problems, motor coordination difficulties and a tendency to bite objects. Following a comprehensive psychiatric evaluation, the patient was diagnosed with developmental coordination disorder, articulation disorder and attention deficit hyperactivity disorder (ADHD). <i>MAOA</i> mutations are rarely reported in the literature. To date, a total of 23 <i>MAOA</i> gene variants, mostly missense variants, have been reported through the HGMD database (Professional 2023.4).</p><p>Neurodevelopmental symptoms may vary in severity and diversity among patients with Brunner syndrome. Different degrees of intellectual disability have been found in previously reviewed cohorts of Brunner syndrome. In our affected patient, cognitive development and academic achievement were at a similar level to his peers. Additionally, our patient exhibited symptoms suggestive of developmental coordination disorder. Our findings show that genetic mutations in <i>MAOA</i> can lead to a wide range of clinical symptoms and underline the need for comprehensive genetic and clinical evaluations.</p>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"84 8","pages":"972-976"},"PeriodicalIF":1.7,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142499847","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":"Role of hsa-miR-543-KIF5C/CALM3 pathway in neuron differentiation of embryonic mesenchymal stem cells","authors":"Dongmei An,&nbsp;Yangfan Wang,&nbsp;Xin Wang","doi":"10.1002/jdn.10386","DOIUrl":"10.1002/jdn.10386","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Human umbilical cord mesenchymal stem cells (hUC-MSCs) have the ability to differentiate into nerve cells, which offers promising options for treating neurodegenerative diseases.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>To explore the important regulatory molecules of hUC-MSCs differentiation into neurons.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method</h3>\u0000 \u0000 <p>In this research, the neural differentiation of hUC-MSCs was induced by a low-serum DMSO/BHA/DMEM medium. The GEO database was used to retrieve the relevant datasets. The starBase and miEAA databases were used for bioinformatics analysis. RT-qPCR was used to detect the hsa-miR-543 level and the mRNA levels of NSE, NeuN, NF-M, KIF5C, and CALM3. The protein levels of KIF5C and CALM3 were checked by western blotting.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The expression levels of NSE, NeuN, NF-M, KIF5C, and CALM3 were elevated, while hsa-miR-543 was under-expressed in neuro-induced hUC-MSCs. The increase in NSE, NeuN, and NF-M mRNA levels induced by DMSO/BHA/DMEM was partially reversed by the knockdown of KIF5C and CALM3 in hUC-MSCs. Moreover, the transfection of hsa-miR-543 mimic partially countered the DMSO/BHA/DMEM-induced elevation in NSE, NeuN, NF-M, KIF5C, and CALM3 mRNA levels.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>KIF5C and CALM3 facilitated the neuronal differentiation of hUC-MSCs, whereas hsa-miR-543 exerted an opposing effect by negatively regulating KIF5C and CALM3.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"84 8","pages":"934-942"},"PeriodicalIF":1.7,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142499869","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":"Cohen syndrome: Can early-onset recurrent infections and hypotonia provide early diagnosis and intervention for intellectual disability?","authors":"Gül Ünsel-Bolat,&nbsp;Ezgi Keskin-Çelebi,&nbsp;Hilmi Bolat","doi":"10.1002/jdn.10384","DOIUrl":"10.1002/jdn.10384","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Cohen syndrome is a rare disease associated with neurodevelopmental disorders, especially intellectual disability (ID), neutropenia and recurrent infections are consistently reported in cases. Neutropenia is an important part of the syndrome, as well as ID. Homozygous variants in the <i>VPS13B</i> gene, located on chromosome 8q22 and containing 62 exons, have been found to cause Cohen syndrome. Cohen syndrome is commonly diagnosed when dysmorphological findings and developmental delay become more apparent. However, the identification of some findings with increasing age has caused the diagnosis of Cohen syndrome to be delayed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Cases diagnosed with ID were evaluated using whole-exome sequencing/clinical exome sequencing method. Family segregation analysis was performed using Sanger sequencing. We presented the clinical and genetic findings of three cases diagnosed with Cohen syndrome and their parents in detail.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In this study, we presented the occurrence of symptoms in different age groups, and the prognosis of three cases carrying the <i>VPS13B</i> gene variants, including three different variant types: missense, frameshift and nonsense. Although our cases had different variant types, they shared important similarities on the onset period and prognosis of the symptoms. All cases presented hypotonia, difficulties in swallowing, recurrent respiratory tract infections, neutropenia, delay in motor development, ID and hyperactivity. Our cases did not have a diagnosis of autism spectrum disorder. All cases had increased willingness to engage in social communication.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>We emphasize the importance of early-onset recurrent infections and hypotonia for early diagnosis and preventive genetic counselling in Cohen syndrome.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"84 8","pages":"918-923"},"PeriodicalIF":1.7,"publicationDate":"2024-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464534","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 review article on the development of dopaminergic neurons and establishment of dopaminergic neuron–based in vitro models by using immortal cell lines or stem cells to study and treat Parkinson's disease","authors":"Azize Yasemin Göksu","doi":"10.1002/jdn.10383","DOIUrl":"10.1002/jdn.10383","url":null,"abstract":"<p>The primary pathological hallmark of Parkinson's disease (PD) is the degeneration of dopaminergic (DA) neurons in the substantia nigra pars compacta, a critical midbrain region. <i>In vitro</i> models based on DA neurons provide a powerful platform for investigating the cellular and molecular mechanisms of PD and testing novel therapeutic strategies. A deep understanding of DA neuron development, including the signalling pathways and transcription factors involved, is essential for advancing PD research. This article first explores the differentiation and maturation processes of DA neurons in the midbrain, detailing the relevant signalling pathways. It then compares various <i>in vitro</i> models, including primary cells, immortalized cell lines, and stem cell-based models, focusing on the advantages and limitations of each. Special attention is given to the role of immortalized and stem cell models in PD research. This review aims to guide researchers in selecting the most appropriate model for their specific research goals. Ethical considerations and clinical implications of using stem cells in PD research are also discussed.</p>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"84 8","pages":"817-842"},"PeriodicalIF":1.7,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390381","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":"Evaluating the potential effects of apigenin on memory, anxiety, and social interaction amelioration after social isolation stress","authors":"Ali Mohammadkhanizadeh,&nbsp;Yasaman Hosseini,&nbsp;Farnaz Nikbakht,&nbsp;Mohammadreza Parvizi,&nbsp;Fatemeh Khodabandehloo","doi":"10.1002/jdn.10380","DOIUrl":"10.1002/jdn.10380","url":null,"abstract":"<p>Vigorous research confirmed the anti-inflammatory, antioxidant, and antidementia effects of apigenin (Api). The present study evaluated the beneficial impacts of Api administration on behaviour, brain-derived neurotrophic factor (BDNF), Interleukin <i>6</i> (IL-6), oxidative stress, and inflammation induced by social isolation (SI) stress in rats. For this purpose, rats underwent a 28-day SI period followed by a 4-week oral Api treatment (50 mg/kg/day, PO). On Day 56, behaviour tests were performed, including an elevated plus maze (EPM), Morris water maze (MWM), and three-chamber social tests. The oxidative stress markers, IL-6, and BDNF levels were measured in the hippocampus. Our results showed that SI stress caused an increase in anxiety and a decrease in spatial memory, sociability, and social preference index. In addition, SI stress increased hippocampal levels of IL-6 and malondialdehyde (MDA) content, whereas it reduced the hippocampal BDNF level and superoxide dismutase (SOD) activities. Our study indicated that Api attenuates anxiety and causes improvements in spatial memory and social interaction. These desirable effects of Api might be related to amelioration in the BDNF level, IL-6, and oxidative stress biomarkers in the hippocampus.</p>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"84 8","pages":"894-904"},"PeriodicalIF":1.7,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142375408","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":"Seizure recurrence following the first unprovoked seizure: Risk factors among children in UAE","authors":"Dina Amin Saleh,&nbsp;Abeera Hassan","doi":"10.1002/jdn.10382","DOIUrl":"10.1002/jdn.10382","url":null,"abstract":"<p>In a retrospective study of paediatric and adolescent patients in Abu Dhabi, UAE, who experienced their first unprovoked seizure between March 2016 and March 2020, with a minimum one-year follow-up, we identified significant risk factors associated with seizure recurrence. Among 317 patients, 96.2% experienced seizure recurrence, with the majority (68.8%) occurring within the first 6-month follow-up period. Notable risk factors for recurrence included focal seizures, symptomatic seizure causes, abnormal initial electroencephalogram (EEG) findings, abnormal brain magnetic resonance imaging results, and the presence of neurological disorders. Interestingly, the type of epileptiform activity in the initial EEG did not predict recurrence risk. Over a 3-year period, the overall recurrence risk was 98.4%, particularly higher in cases with symptomatic seizures compared to idiopathic (genetic) ones. These findings underscore the importance of vigilant monitoring, particularly in the early post-seizure follow-up period, and advocate for initial EEG assessments, especially in cases of remote symptomatic first unprovoked seizures.</p>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"84 8","pages":"905-917"},"PeriodicalIF":1.7,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142371785","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}