International Journal of Developmental Neuroscience最新文献

{"title":"Therapeutic effects of nanosilibinin in valproic acid-zebrafish model of autism spectrum disorder: Focusing on Wnt signaling pathway and autism spectrum disorder-related cytokines","authors":"Zahra Karimi,&nbsp;Asadollah Zarifkar,&nbsp;Esmaeil Mirzaei,&nbsp;Mehdi Dianatpour,&nbsp;Mahintaj Dara,&nbsp;Hadi Aligholi","doi":"10.1002/jdn.10348","DOIUrl":"10.1002/jdn.10348","url":null,"abstract":"<p>In this study, we delved into the intricate world of autism spectrum disorder (ASD) and its connection to the disturbance in the Wnt signaling pathway and immunological abnormalities. Our aim was to evaluate the impact of silibinin, a remarkable modulator of both the Wnt signaling pathway and the immune system, on the neurobehavioral and molecular patterns observed in a zebrafish model of ASD induced by valproic acid (VPA). Because silibinin is a hydrophobic molecule and highly insoluble in water, it was used in the form of silibinin nanoparticles (nanosilibinin, NS). After assessing survival, hatching rate, and morphology of zebrafish larvae exposed to different concentrations of NS, the appropriate concentrations were chosen. Then, zebrafish embryos were exposed to VPA (1 μM) and NS (100 and 200 μM) at the same time for 120 h. Next, anxiety and inattentive behaviors and the expression of CHD8, CTNNB, GSK3beta, LRP6, TNFalpha, IL1beta, and BDNF genes were assessed 7 days post fertilization. The results indicated that higher concentrations of NS had adverse effects on survival, hatching, and morphological development. The concentrations of 100 and 200 μM of NS could ameliorate the anxiety-like behavior and learning deficit and decrease ASD-related cytokines (IL1beta and TNFalpha) in VPA-treated larvae. In addition, only 100 μM of NS prevented raising the gene expression of Wnt signaling-related factors (CHD8, CTNNB, GSK3beta, and LRP6). In conclusion, NS treatment for the first 120 h showed therapeutic effect on an autism-like phenotype probably via reducing the expression of pro-inflammatory cytokines genes and changing the expression of Wnt signaling components genes.</p>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"84 5","pages":"454-468"},"PeriodicalIF":1.7,"publicationDate":"2024-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141497987","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":"Neurocognitive features in childhood & adulthood in autism spectrum disorder: A neurodiversity approach","authors":"Dr. Kalliopi Megari,&nbsp;Chionia K. Frantzezou,&nbsp;Zoi A. Polyzopoulou,&nbsp;Stella K. Tzouni","doi":"10.1002/jdn.10356","DOIUrl":"10.1002/jdn.10356","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>Autism spectrum disorder (ASD) is a neurodevelopmental disorder with a diverse profile of cognitive functions. Heterogeneity is observed among both baseline and comorbid features concerning the diversity of neuropathology in autism. Symptoms vary depending on the developmental stage, level of severity, or comorbidity with other medical or psychiatric diagnoses such as intellectual disability, epilepsy, and anxiety disorders.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method</h3>\u0000 \u0000 <p>The neurodiversity movement does not face variations in neurological and cognitive development in ASD as deficits but as normal non-pathological human variations. Thus, ASD is not identified as a neurocognitive pathological disorder that deviates from the typical, but as a neuro-individuality, a normal manifestation of a neurobiological variation within the population.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In this light, neurodiversity is described as equivalent to any other human variation, such as ethnicity, gender, or sexual orientation. This review will provide insights about the neurodiversity approach in children and adults with ASD. Using a neurodiversity approach can be helpful when working with children who have autism spectrum disorder (ASD).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Discussion</h3>\u0000 \u0000 <p>This method acknowledges and values the various ways that people with ASD interact with one another and experience the world in order to embrace the neurodiversity approach when working with children with ASD.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"84 6","pages":"471-499"},"PeriodicalIF":1.7,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141491849","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":"Ethyl pyruvate alleviates NLRP3/Caspase-1/GSDMD-mediated neuronal pyroptosis in neonatal rats with hypoxic–ischemic brain damage","authors":"Sha Sha,&nbsp;Ni Jin,&nbsp;Xinyi Xie,&nbsp;Ruiyu Zhou,&nbsp;Yanghao Ruan,&nbsp;Ying Ouyang","doi":"10.1002/jdn.10357","DOIUrl":"10.1002/jdn.10357","url":null,"abstract":"<p>Pyroptosis is an inflammation-associated programmed cell death, and neuroinflammation is strongly associated with severe neurological deficits in neonatal hypoxic–ischemic encephalopathy (HIE). Ethyl pyruvate (EP), a known anti-inflammatory agent, has shown promise in the treatment of hypoxic–ischemic brain damage (HIBD) rats; nevertheless, the therapeutic mechanism of EP and its capacity to suppress neuronal pyroptosis in HIBD rats remain unclear. In both the neonatal Rice-Vannucci rat model and the OGD/R model, this study examined alterations in the NLRP3/Caspase-1/GSDMD classical pyroptosis pathway in hippocampal neurons during HIE and the potential inhibitory impact of ethyl pyruvate on this pathway. We used HE staining, immunofluorescence double staining, transmission electron microscopy, and western blot to demonstrate that EP effectively inhibited hippocampal neuronal pyroptosis and attenuated the activation of the NLRP3/Caspase-1/GSDMD signaling pathway in HIBD rats, which resulted in a reduction of neuroinflammation and facilitated neural recovery. The results suggest that EP may be a promising neuroprotective agent for treating HIE.</p>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"84 6","pages":"594-604"},"PeriodicalIF":1.7,"publicationDate":"2024-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141467827","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":"CircNUP98 promotes the malignant behavior of glioma cells through the miR-520f-3p/ELK4 axis","authors":"Liangqin Nie,&nbsp;Tianyu Jiang","doi":"10.1002/jdn.10355","DOIUrl":"10.1002/jdn.10355","url":null,"abstract":"<p>Glioma, a formidable form of brain cancer, poses significant challenges in terms of treatment and prognosis. Circular RNA nucleoporin 98 (circNUP98) has emerged as a potential regulator in various cancers, yet its role in glioma remains unclear. Here, we elucidate the functional role of circNUP98 in glioma cell proliferation, invasion, and migration, shedding light on its therapeutic implications. Glioma cells were subjected to si-NUP98 transfection, followed by assessments of cell viability, proliferation, invasion, and migration. Subcellular localization of circNUP98 was determined, and its downstream targets were identified. We delineated the binding relationships between circNUP98 and microRNA (miR)-520f-3p, as well as between miR-520f-3p and ETS transcription factor ELK4 (ELK4). The expression levels of circNUP98/miR-520f-3p/ELK4 were quantified. Our findings demonstrated that circNUP98 was upregulated in glioma cells, and its inhibition significantly attenuated glioma cell proliferation, invasion, and migration. Mechanistically, circNUP98 functioned as a sponge for miR-520f-3p, thereby relieving the inhibitory effect of miR-520f-3p on ELK4. Moreover, inhibition of miR-520f-3p or overexpression of ELK4 partially rescued the suppressive effect of circNUP98 knockdown on glioma cell behaviors. In summary, our study unveils that circNUP98 promotes glioma cell progression via the miR-520f-3p/ELK4 axis, offering novel insights into the therapeutic targeting of circNUP98 in glioma treatment.</p>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"84 6","pages":"581-593"},"PeriodicalIF":1.7,"publicationDate":"2024-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141456584","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":"Dysregulation of miR-146a in human milk of mothers having children with autism","authors":"Nagwa A. Meguid,&nbsp;Maha Hemimi,&nbsp;Mahmoud Rashad,&nbsp;Amal Elsaeid,&nbsp;Gina Elpatrik,&nbsp;Hala M. Zeidan","doi":"10.1002/jdn.10353","DOIUrl":"10.1002/jdn.10353","url":null,"abstract":"<p>Autism spectrum disorder (ASD) is a set of neurobehavioral manifestations that impose poor social interaction and stereotyped repetitive patterns. Several mircoRNA (miRNA) dysregulations underpin ASD pathophysiology via impairing the neurogenic niches. For instance, miR-146a and miR-106 differential expressions are linked to deregulation of ASD-related genes and the severity of clinical symptoms, respectively. Breastfeeding provides newborns with many bioactive compounds that support their neurodevelopment including miRNA. Our pilot study evaluated the expression pattern of miR-106a and miR-146a in human milk (HM) of nursing mothers (<i>n</i> = 36) having autistic children compared to age-matched counterparts (<i>n</i> = 36) with neurotypical children as controls. Under sterile conditions, breast milk samples were collected using manual sucking pumps and centrifuged to separate the fat layer. Total RNA was extracted from the lipid fraction, and the expression profiles of both miR-106a and miR-146a were evaluated using quantitative real-time polymerase chain reaction. Among the test group, we reported some factors that were previously linked to HM miRNA perturbations: gestational diabetes, hypertension, and cesarean delivery. HM miR-106a showed comparable expression levels in both mother groups (<i>p</i> = 0.8681), whereas HM miR-146a was significantly downregulated in mothers with autistic children compared to controls (<i>p</i> = 0.0399). Alternatively, HM miR-106 levels were positively associated with two ASD clinical parameters: Childhood Autism Rating Scale (CARS) and communication and language domain of Autism Diagnostic Interview-Revised (ADI-R) (<i>r</i> = 0.6452, <i>p</i> = 0.0003 and <i>r</i> = 0.3958, <i>p</i> = 0.0410, respectively). The receiver operating characteristic (ROC) curves of both maternal HM miR-106a and miR-146a showed poor fitness as predictive biomarkers for ASD. Our findings suggest that the miR-146a differential expression in ASD children may originate at infancy during the lactation period. Thus, maternal pre- and postnatal health care is critical to maintain optimal miRNome in breast milk.</p>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"84 6","pages":"558-566"},"PeriodicalIF":1.7,"publicationDate":"2024-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141456585","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":"Supplementation with stigma maydis polysaccharide attenuates autism-like behaviors and improves gut function in valproic acid-induced autism model male rats","authors":"Xiaolei Yang,&nbsp;Hongjie Li,&nbsp;Chao Yang,&nbsp;Jie Ge","doi":"10.1002/jdn.10354","DOIUrl":"10.1002/jdn.10354","url":null,"abstract":"<p>Stigma maydis polysaccharide (SMPS) has regulatory effect on the intestinal microflora and promotes gastrointestinal peristalsis. Children with autism spectrum disorder (ASD) often experience gastrointestinal problems and dysbiosis in their gut microbiota. Our previous study revealed that SMPS interventions had an impact on the gut microbiota of valproic acid (VPA)-induced autism model rats. However, the effects of SMPS on the behavior and gut function of autism model rats remain poorly understood. Therefore, we gave different doses of SMPS intervention in the early stage of autism model rats to observe their developmental conditions and behavior performances. Through histological evaluation and real-time polymerase chain reaction (PCR), integrity of the intestinal structure and the expression of tight junction-related gene <i>Zo-1</i> and <i>Occludin</i> were detected. The results indicated that SMPS intervention improved the physical development, learning and memory impairment, and social performance of autism model rats. Meanwhile, SMPS promoted intestinal peristalsis and restored the integrity of the intestinal structure, reduced the number of inflammatory cells, and increased the expression of the <i>Zo-1</i> and <i>Occludin</i> genes. Furthermore, the expression levels of neurotransmitters (substance P, enkephalin, vasoactive intestinal peptide, and 5-hydroxytryptamine) in the hippocampal tissues were altered after SMPS treatment. In conclusion, SMPS could ameliorate ASD-like phenotypes and gut problems in autism model rats. Collectively, these results provide new evidence for the relationship between the gut-brain axis and ASD and suggest a novel therapeutic target for ASD treatment.</p>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"84 6","pages":"567-580"},"PeriodicalIF":1.7,"publicationDate":"2024-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141456586","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 and postnatal cocaine exposure enhances the anxiety- and depressive-like behaviors in rats: An ontogenetic study","authors":"Susana Barbosa Méndez,&nbsp;Alberto Salazar-Juárez","doi":"10.1002/jdn.10358","DOIUrl":"10.1002/jdn.10358","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Prenatal and postnatal exposure to drugs such as cocaine is a public health problem that causes deficits in brain development and function in humans and animals. One of the main effects of prenatal and postnatal cocaine exposure is increased vulnerability to developing the substance use disorder at an early age. Furthermore, the negative emotional states associated with cocaine withdrawal increase the fragility of patients to relapse into drug abuse. In this sense, prenatal and postnatal cocaine exposure enhanced the cocaine- and nicotine-induced locomotor activity and locomotor sensitization, and rats exposed prenatally to cocaine displayed an increase in anxiety- and depressive-like behaviors in adulthood (PND 60–70).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Therefore, the objective of this study was to determine the effect of prenatal and postnatal cocaine exposure on anxiety- and depressive-like behaviors at different ages (30, 60, 90, and 120 days of age) in rats.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The study was divided into two stages: prenatal and postnatal. In the prenatal stage, a group of pregnant female Wistar rats was administered daily from GD0 to GD21 cocaine (cocaine pre-exposure group), and another group of pregnant female rats was administered daily saline (saline pre-exposure group). In the postnatal stage, during lactation (PND0 to PND21), pregnant rats received administration of cocaine or saline, respectively. Of the litters resulting from the cocaine pre-exposed and saline pre-exposed pregnant female groups, only the male rats were used for the recording of the anxiety- and depressive-like behaviors at different postnatal ages (30, 60, 90, and 120 days), representative of adolescence, adult, adulthood, and old age.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The study found that prenatal and postnatal cocaine exposure generated age-dependent enhancement in anxiety- and depressive-like behaviors, being greater in older adult (PND 120) rats than in adolescent (PND 30) or adults (PND 60–90) rats.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This suggests that prenatal and postnatal cocaine exposure increases anxiety- and depressive-like behaviors, which may increase the vulnerability of subjects to different types of drugs in young and adult age.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"84 6","pages":"546-557"},"PeriodicalIF":1.7,"publicationDate":"2024-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141515221","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":"Rhein inhibits M1 polarization of BV2 microglia through MAPK/IκB signalling pathway and reduces neurotoxicity caused by neuroinflammation","authors":"Xin Qin,&nbsp;Bowen Li,&nbsp;Binbin Hu,&nbsp;Juan Huang,&nbsp;Xingfu Tian,&nbsp;Xinyue Zhang,&nbsp;Ye Wang,&nbsp;Wei Huang","doi":"10.1002/jdn.10352","DOIUrl":"10.1002/jdn.10352","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Rhein is an anthraquinone compound with anti-inflammatory pharmacological activity. It has been found to play a neuroprotective role in neurological diseases, but the neuroprotective mechanism of rhein remains unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>SH-SY5Y cells serving as neuron-like cells and BV2 microglia were used. The toxicity of rhein on BV2 microglia and the viability of SH-SY5Y cells were measured by CCK-8 assay. The mRNA expression and secretion of pro-inflammatory cytokines were detected by qPCR and ELISA. Iba1, CD86 and pathway signalling protein in BV2 microglia were assessed by Western blot and immunofluorescence. Apoptosis of SH-SY5Y cells exposed to neuroinflammation was analysed through flow cytometry.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Rhein inhibited MAPK/IκB signalling pathways. Further studies revealed that rhein inhibited the production of pro-inflammatory cytokines TNF-α, IL-6, IL-1β and iNOS in BV2 cells and also inhibited the expression of M1 polarization markers Iba1 and CD86 in BV2 cells. Furthermore, rhein reduced the apoptotic rate and restored cell viability of SH-SY5Y cells exposed to neuroinflammation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our study demonstrated that rhein inhibited microglia M1 polarization via MAPK/IκB signalling pathway and protected nerve cells through suppressing neuroinflammation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"84 6","pages":"533-545"},"PeriodicalIF":1.7,"publicationDate":"2024-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141300593","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":"Melatonin attenuates developmental deficits and prevents hippocampal injuries in male and female rats subjected to neonatal anoxia","authors":"Bruna Petrucelli Arruda,&nbsp;Natalia Andrea Cruz-Ochoa,&nbsp;Fernando Tadeu Serra,&nbsp;Gilberto Fernando Xavier,&nbsp;Maria Inês Nogueira,&nbsp;Silvia Honda Takada","doi":"10.1002/jdn.10351","DOIUrl":"10.1002/jdn.10351","url":null,"abstract":"<p>Hypoxia in preterm infants is a clinical condition that has been associated with cognitive and behavioral disturbances for which treatment strategies are strongly required. Melatonin administration following brain insults has been considered a promising therapeutic strategy due to its antioxidant and anti-inflammatory effects. Not surprisingly, it has been extensively studied for preventing disturbances following brain injury. This study evaluated the effects of melatonin on developmental disturbances, memory disruption, and hippocampal cell loss induced by neonatal anoxia in rats. Neonatal Wistar rats were subjected to anoxia and subsequently treated with melatonin. Later, maturation of physical characteristics, ontogeny of reflexes, learning and memory in the Morris water maze (MWM), and estimates of the number of hippocampal neurons, were evaluated. Melatonin treatment attenuated (1) female anoxia-induced delay in superior incisor eruption, (2) female anoxia-induced vibrissae placement reflexes, and (3) male and female anoxia-induced hippocampal neuronal loss. Melatonin also promoted an increase (5) in swimming speeds in the MWM. In addition, PCA analysis showed positive associations between the acoustic startle, auditory canal open, and free fall righting parameters and negative associations between the male vehicle anoxia group and the male melatonin anoxia group. Therefore, melatonin treatment attenuates both anoxia-induced developmental deficits and hippocampal neuronal loss.</p>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"84 6","pages":"520-532"},"PeriodicalIF":1.7,"publicationDate":"2024-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141300592","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":"Hot and cold executive function among pediatric attention deficit hyperactivity disorder with and without coexisting oppositional defiant disorder","authors":"Nasim Kamalahmadi,&nbsp;Fatemeh Moharrari,&nbsp;Atefeh Soltanifar,&nbsp;Saeedeh Hajebi Khaniki,&nbsp;Hossein Mohaddes,&nbsp;Ghazaleh Noorbakhsh,&nbsp;Razie Salehabadi","doi":"10.1002/jdn.10346","DOIUrl":"10.1002/jdn.10346","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Executive function is a high-level set of cognitive processes related to goal-directed behaviors including two conceptual subtypes of hot (emotional) and cold (cognitive) executive function (to abbreviate EF). EF deficits in attention deficit hyperactivity disorder (ADHD) leads to significant social impairments in the home, school, and community. Today the type and the extent of executive function defects in ADHD are still debated in studies. We aimed to evaluate hot and cold executive function among medication-naive children with ADHD, with and without oppositional defiant disorder (ODD).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Forty-five children including suffering ADHD with ODD (<i>n</i> = 15), without ODD (<i>n</i> = 15), or typically developed (TD, <i>n</i> = 15) participated in this cross-sectional study (the age of children was between 7 and 12 years old). The Child Symptom Inventory-4 (CSI-4) was used to screen behavioral and emotional symptoms. Wechsler Adult Intelligence Scale-Revised-Digit Span Task (WAIS-R-DST), Corsi Block Task (CBT), and Wisconsin Card Sorting Test (WCST) were used for assessing cold executive function. Assessing hot executive function was done with Delay Discounting Task (DDT) and Iowa Gambling Task (IGT).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Evaluating the cold executive function, total WAIS-R-DST score, Backward DST, total CBT score, and Backward CBT were significantly lower among ADHD than TD groups (<i>p</i> &lt; 0.05). Assessing the hot executive function showed that the score of DDT and IGT was significantly lower among ADHD than TD groups (<i>p</i> &lt; 0.05).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Both hot and cold executive functions are defective in children with ADHD, while the comorbid of ODD has no significant effect. We suggest the clinicians to consider cognitive rehabilitation interventions as a necessary treatment modality for ADHD patients.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"84 5","pages":"446-453"},"PeriodicalIF":1.7,"publicationDate":"2024-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141237386","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}