Journal of Molecular Neuroscience最新文献

{"title":"Oxidative Stress and Dynamic Thiol/Disulfide Homeostasis in Autism: A Focus on Early Childhood","authors":"Halenur Teke,&nbsp;Senay Balci,&nbsp;Salim Neselioglu,&nbsp;Selçuk Teke,&nbsp;Ozcan Erel,&nbsp;Lulufer Tamer,&nbsp;Fevziye Toros","doi":"10.1007/s12031-025-02358-z","DOIUrl":"10.1007/s12031-025-02358-z","url":null,"abstract":"<div><p>Autism spectrum disorder (ASD) is a complex neurodevelopmental condition with multifactorial etiopathogenesis, where oxidative stress (OS) has been implicated as a key contributing factor. This study aimed to evaluate the plasma dynamic thiol/disulfide homeostasis (DTDH) parameters—a relatively novel OS biomarker—alongside classical OS biomarkers, including total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), glutathione, and glutathione peroxidase (GPx), in preschool children diagnosed with ASD. A total of 49 children with ASD and 31 age- and sex-matched typically developing children between the ages of 2 and 6 years were included. In addition to sociodemographic data collection, the Childhood Autism Rating Scale (CARS) and Clinical Global Impression-Severity Scale (CGI-S) were administered to assess autism severity. Blood samples were analyzed using automated spectrophotometric techniques to determine OS biomarkers. The results demonstrated that DTDH parameters and classical OS markers exhibited parallel changes; however, no statistically significant differences were detected between the ASD and control groups across all OS markers. Furthermore, no significant association was found between OS biomarkers and autism severity. Moreover, we intentionally restricted our sample to a younger age group to enable a focused examination of OS dynamics during early developmental stages. This study underscores the potential impact of age as a critical determinant in OS-related alterations in autism and highlights the need for further age-stratified investigations to elucidate the role of OS in ASD pathophysiology and its potential diagnostic relevance.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s12031-025-02358-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143900739","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":"Discovering Novel Biomarkers and Potential Therapeutic Targets of Amyotrophic Lateral Sclerosis Through Integrated Machine Learning and Gene Expression Profiling","authors":"Farah Anjum,&nbsp;Abdulaziz Alsharif,&nbsp;Maha Bakhuraysah,&nbsp;Alaa Shafie,&nbsp;Md.Imtaiyaz Hassan,&nbsp;Taj Mohammad","doi":"10.1007/s12031-025-02340-9","DOIUrl":"10.1007/s12031-025-02340-9","url":null,"abstract":"<div><p>Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder that has multiple factors that make its molecular pathogenesis difficult to understand and its diagnosis and treatment during the early stages difficult to determine. Discovering novel biomarkers in ALS for diagnostic and therapeutic potential has become important. Consequently, bioinformatics and machine learning algorithms are useful for identifying differentially expressed genes (DEGs) and potential biomarkers, as well as understanding the molecular mechanisms and intricacies of diseases such as ALS. To achieve the aim of the present study, six datasets obtained from the Gene Expression Omnibus (GEO) were utilized and analyzed using an integrative bioinformatics and machine learning approach. Log transformation was done during data preprocessing, RMA normalization was performed, and the batch effect was corrected. Differential expression analysis identified 206 DEGs that were significantly associated with different biological processes, including muscle function, energy metabolism, and mitochondrial membrane activity. Functional enrichment analysis highlighted pathways, including those related to prion disease, Parkinson’s disease, and ATP synthesis via chemiosmotic coupling. We employed a multi-step machine learning framework incorporating random forest, LASSO regression, and SVM-RFE to identify robust biomarkers. This approach identified three key genes, <i>CHRNA1</i>, <i>DLG5</i>, and <i>PLA2G4C</i>, which could be explored as promising biomarkers for ALS after further validation. The internal validation, including principal component analysis (PCA) and ROC-AUC analysis, demonstrated strong diagnostic potential of these hub genes, achieving an AUC of 0.96. This work highlights the utility of bioinformatics and machine learning in identifying key genes as biomarkers for diagnostic and therapeutic potential in ALS.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143888613","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":"Identification and Validation of Glycosylation‑Related Genes in Ischemic Stroke Based on Bioinformatics and Machine Learning","authors":"Hui Zhang,&nbsp;Yanan Ji,&nbsp;Zhongquan Yi,&nbsp;Jing Zhao,&nbsp;Jianping Liu,&nbsp;Xianxian Zhang","doi":"10.1007/s12031-025-02352-5","DOIUrl":"10.1007/s12031-025-02352-5","url":null,"abstract":"<div><p>Ischemic stroke (IS) constitutes a severe neurological disorder with restricted treatment alternatives. Recent investigations have disclosed that glycosylation is closely associated with the occurrence and outcome of IS. Nevertheless, data on the transcriptomic dynamics of glycosylation in IS are lacking. The objective of this study was to undertake a comprehensive exploration of glycosylation-related genes (GRGs) in IS via bioinformatics and to assess their immune characteristics. In this study, through the intersection of genes from weighted gene co-expression network analysis, GRGs from five glycosylation pathways, and DEGs from differential expression analysis, 20 candidate GRGs were identified. Subsequently, through LASSO, Random Forest, and SVM-RFE, 3 hub GRGs (F5, PPP6C, and UBE2J1) were identified. Additional, a gene diagnostic model linked to glycosylation was developed and validated. The findings indicated that the diagnostic model could effectively distinguish between IS patients and healthy individuals in the training, validation, and merging datasets, indicating clinical relevance. Subsequently, by employing unsupervised clustering analysis, IS patients were classified into three clusters, and significant disparities were witnessed in immune cell infiltration among distinct clusters. In summary, this study successfully identified hub GRGs in IS and investigated the roles of these hub genes in the immune microenvironment, indicating potential clinical applications for IS.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143888747","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":"Ursolic Acid and Caprylic Acid Cocktail Approach Against Pentylenetetrazole-induced Seizures-like Behavior in Adult Zebrafish: Preclinical Study","authors":"Deepali Sharma,&nbsp;Simranjeet Walia,&nbsp;Simranjit Kaur,&nbsp;Lakshay Kapil,&nbsp;Charan Singh,&nbsp;Arti Singh","doi":"10.1007/s12031-024-02289-1","DOIUrl":"10.1007/s12031-024-02289-1","url":null,"abstract":"<div><p>Epilepsy is a neurological disorder characterized by recurrent seizures. Pentylenetetrazole (PTZ) is a chemoconvulsant that impairs GABAergic and glutamatergic neurotransmission, promoting excitotoxicity and seizures. Ursolic acid (UA) and caprylic acid (CA) have anti-inflammatory, anti-oxidant, and neuroprotective properties. The objective of the present study was to investigate the combined effect of UA and CA on seizures, neuronal damage, and inflammation induced by PTZ in adult zebrafish. Adult zebrafish (~6-8 months old; 470-530 mg, n=20) were randomly assigned to 10 different groups namely- I) vehicle: 10% DMSO (20µl/kg, <i>i.p</i>), II) Diazepam 1.25 mg/kg <i>per se</i> (DZP, <i>i.p</i>), III) UA 150 mg/kg <i>per se</i> (<i>i.p</i>), IV) CA 60 mg/kg <i>per se</i> (<i>i.p</i>), V) PTZ 170 mg/kg (<i>i.p</i>), VI) DZP 1.25 + PTZ 170 (30 min after DZP 1.25), VII) UA 50 + PTZ 170 (30 min after UA 50), VIII) UA 150 + PTZ 170 (30 min after UA 150), IX) CA 60 + PTZ 170 (30 min after CA 60), and X) UA 50 and CA 60 + PTZ 170 (30 min after UA 50 and CA 60) administration followed by seizure scoring, neurobehavioral (Novel tank test and open field test), biochemical [lipid peroxidase (LPO), acetylcholinesterase (AChEs), superoxide dismutase catalase (SOD), and glutathione-s-transferase (GSH)], molecular (TNF-α, IL-10, Nrf-2 and IL-1β), mitochondrial (complex I, II, IV), cell viability assay (MTT assay) and histopathological analysis. UA of both doses and CA decreased mean seizure score, and mean seizure time. Importantly, combination of UA 50 mg/kg and CA 60 mg/kg attenuated seizure-like behavioural scores, decreased mean seizure time, mean seizure score and reduced the frequency of clonic-like seizures (score 4) in PTZ-treated zebrafish. A combination of UA 50 mg/kg and CA 60 mg/kg also prevented oxidative stress in PTZ-challenged fish by decreasing lipid peroxidation, AChEs activity and increasing catalase, GSH and SOD levels. Additionally, the combination therapy prevented inflammatory response by declining TNF-α and IL-1β levels and raising IL-10 and Nrf-2 levels. Moreover, combination of UA 50 mg/kg and CA 60 mg/kg significantly improved mitochondrial complex I, II and IV activities as well as increase mitochondrial viability in MTT assay. Furthermore, morphology of neuronal cell was prevented in combination of UA 50 mg/kg and CA 60 mg/kg as seen in H &amp; E staining. The protective effect of UA 50 mg/kg and CA 60 mg/kg cocktail is comparable with standard drug Diazepam. Together, we demonstrate that UA 50 mg/kg and CA 60 mg/kg cocktail significantly attenuated PTZ-induced seizure-like behaviours, brain oxidative stress, mitochondrial dysfunction and morphological damage of neuronal cell in zebrafish, suggesting the involvement of its strong anti-inflammatory and antioxidant mechanisms in neuroprotection.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143879683","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":"Sex Hormone-Related Pathogenic Genes in Multiple Sclerosis: A Multi-omics Mendelian Randomization Study","authors":"Jiting Qiu,&nbsp;Yuwen Zhang","doi":"10.1007/s12031-025-02347-2","DOIUrl":"10.1007/s12031-025-02347-2","url":null,"abstract":"<div><p>Multiple sclerosis (MS) is a chronic autoimmune disease with complex etiologies, including genetic factors. Sex hormones have been implicated in MS pathogenesis, but the underlying genetic mechanisms remain unclear.This study employed a multi-omics Mendelian randomization (MR) approach to evaluate the causal associations between sex hormone-related genes and MS. We utilized summary data from genome-wide association studies (GWAS) and blood-based methylation quantitative trait loci (mQTLs), expression QTL (eQTLs), and proteomic QTL (pQTLs). The analysis employed the summary data-based MR (SMR) method and the HEIDI test for pleiotropy. Colocalization analysis identified shared genetic determinants, validated in UK Biobank and FinnGen R10 cohort. Our study identified a total of 30 mQTLs and 15 eQTLs that confirmed the causal associations between sex hormone-related genes and MS by SMR and colocalization analyses. Notably, the methylation site cg19286687 of the <i>DES</i> gene was positively associated with MS risk. Similarly, <i>DES</i> expression was positively associated with MS risk in eQTL data. Integration of mQTL and eQTL data revealed a positive regulatory association between cg19286687 and <i>DES</i> expression, suggesting that low methylation level of cg19286687 may inhibit <i>DES</i> expression, potentially contributing to MS risk reduction. This multi-omics MR study suggests a potential causal association between sex hormone-related genes and MS. The findings highlight the importance of <i>DES</i> and its methylation the pathogenesis of MS, offering new ideas on disease mechanisms.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143877703","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":"Unraveling the Complexity of Alzheimer’s Disease: Insights into Etiology and Advancements in Treatment Strategies","authors":"Bakhtawar Khan,&nbsp;Muhammad Khalid Iqbal,&nbsp;Muhammad Ajmal Khan,&nbsp;Hamid Khan,&nbsp;Mubin Mustafa Kiyani,&nbsp;Shahid Bashir,&nbsp;Shao Li","doi":"10.1007/s12031-025-02337-4","DOIUrl":"10.1007/s12031-025-02337-4","url":null,"abstract":"<div><p>Alzheimer’s disease, a complex and progressive neurological disorder, is the leading cause of late-life dementia. Pathologically, it is marked by the presence of amyloid plaques and neurofibrillary tangles in the brain. Over the past two decades, advancements in understanding the disease’s pathogenesis have spurred research into new pharmacological treatments that target its underlying mechanisms. Currently available drugs, such as acetylcholinesterase inhibitors (rivastigmine, galantamine, donepezil) and the NMDA receptor antagonist memantine, primarily address symptoms and are effective only in the later stages of the disease. While these medications can slow disease progression and provide symptomatic relief, they do not offer a cure. Despite having a clear understanding of Alzheimer’s neuropathology, the precise mechanisms driving the disease remain elusive. The lack of effective treatments that can stop the start and progression of the disease may be caused by our incomplete understanding of the pathogenic process. New therapeutic targets are now available due to the significant advancements made in pathophysiology over the past few years, which should allow for a direct attack on the underlying illness process. The various pathophysiological pathways that underlie Alzheimer’s disease and how it is managed by conventional medication therapy, including current exploratory therapeutic options, are covered in this review article. Innovative, beneficial policies are essential to determine and progress therapeutic molecules to defend against AD.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143871334","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":"UCHL1-Mediated Spastin Degradation Regulates Microtubule Severing and Hippocampal Neurite Outgrowth","authors":"Ao Ma,&nbsp;Zhi Liang,&nbsp;Hongde Zhang,&nbsp;Zhichao Meng,&nbsp;Jiehao Zhu,&nbsp;Shu Chen,&nbsp;Qisheng Lin,&nbsp;Tao Jiang,&nbsp;Minghui Tan","doi":"10.1007/s12031-025-02348-1","DOIUrl":"10.1007/s12031-025-02348-1","url":null,"abstract":"<div><p>As a key component of the cytoskeleton, microtubule dynamic provides structural support for neurite outgrowth. Spastin, a microtubule severing enzyme associated with hereditary spastic paraplegia (HSP), is crucial for the growth and branching of neuronal processes. Thus, the activity and function of spastin need to be strictly regulated. However, the mechanism by which spastin protein levels are regulated is still poorly understood. In the current study, we showed that UCHL1 interacted with spastin via mass spectrometry, GST-pulldown and immunoprecipitation assays. Overexpression of UCHL1 decreased the protein level of spastin, while the genetic knockdown of UCHL1 increased that of spastin. CHX chase assay showed that UCHL1 regulated the protein degradation of spastin. Application of proteasome inhibitor MG-132 suppressed UCHL1-mediated spastin degradation. Furthermore, overexpression or knockout of UCHL1 can inhibit or restore spastin-mediated microtubule severing, thereby regulating neuronal length and branch formation. These findings reveal the important regulatory mechanism of UCHL1 on spastin-mediated neurite outgrowth.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143871156","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":"Causal Association Between Sleep Deprivation and Glioblastoma Risk: Insights from Multi-Omics Analysis","authors":"Runze Du,&nbsp;Mulade Maierdan,&nbsp;Aierpati Yusufu,&nbsp;Shiming Dong,&nbsp;Xiaoyu Cai,&nbsp;Tao Xu,&nbsp;Weibin Sheng,&nbsp;Maierdan Maimaiti","doi":"10.1007/s12031-025-02354-3","DOIUrl":"10.1007/s12031-025-02354-3","url":null,"abstract":"<div><p>Emerging evidence suggests that sleep deprivation may contribute to cancer risk. However, the genetic association between sleep deprivation and glioblastoma (GBM) remains unexplored. This study aimed to investigate the causal relationship between sleep traits and GBM using genome-wide association study (GWAS) data of sleep duration, sleeplessness, GBM, and immune cell traits from the UK Biobank and FinnGen databases. Mendelian randomization (MR) analyses were conducted to assess potential causal links between sleep traits and GBM risk. Mediation analysis was performed to identify immune mediators affected by sleep duration that might influence GBM development. Single-nucleus RNA sequencing (snRNA-seq) was utilized to examine cellular subpopulation changes in brain tissue from sleep-deprived (<i>SD</i>) and ad libitum sleep mice. Additionally, a mouse model of sleep deprivation was established for transcriptomic analysis. We found a significant causal association between reduced sleep duration and increased GBM risk (<i>IVW OR</i> = 6.000 × 10⁻⁵, <i>P</i> = 0.003, Bonferroni <i>P</i> = 0.025). Sleeplessness also emerged as a potential risk factor for GBM <i>(OR-IVW</i> = 20.221, <i>P</i> = 0.038). Mediation analysis identified CD80 expression on plasmacytoid dendritic cells (pDCs) as a mediator in the association between sleep duration and GBM, with a mediation effect of 0.256. SnRNA-seq confirmed significant alterations in CD80 + pDCs in sleep-deprived mice. Transcriptomic analysis of SD mice demonstrated upregulation of GBM-related markers (Egfr, Tert, and Mgmt) and associated signaling pathways. These findings suggest a potential causal link between insufficient sleep and increased GBM risk, highlighting the importance of sleep management for GBM patients.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s12031-025-02354-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143871157","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":"MiR- 142 - 3p Up-regulation Mitigates Cerebral Ischemia–reperfusion Injury by Targeting PICALM","authors":"Lili Xie,&nbsp;Debin Yuan,&nbsp;Qian Li,&nbsp;Nan Gu,&nbsp;Haicun Shi,&nbsp;Jianguo Zhong,&nbsp;Fuling Yan","doi":"10.1007/s12031-025-02351-6","DOIUrl":"10.1007/s12031-025-02351-6","url":null,"abstract":"<div><p>Research has shown that miR-142-3p is vital in numerous ischemic diseases and is strongly linked to apoptosis. The effects and precise mechanisms behind miR-142-3p in cerebral ischemia–reperfusion injury (CIRI) are not yet comprehensively elucidated. The results revealed significant repression in miR-142-3p and elevation in PICALM in the plasma of CIRI individuals. To explore further, middle cerebral artery occlusion (MCAO) rat models and oxygen–glucose deprivation/reoxygenation (OGDR)-induced SH-SY5Y cells were conducted. In brain tissue and SH-SY5Y cells, we employed qRT-PCR and Western blot (WB) to estimate miR-142-3p alongside PICALM expression. Notably, overexpression of miR-142-3p significantly minimized infarct areas and cell apoptosis in ischemic rats, as evidenced by TTC staining and immunohistochemistry. Similarly, miR-142-3p upregulation enhanced cell viability (CV) while suppressing SH-SY5Y cell death under OGDR conditions. The connection between miR-142-3p and PICALM was validated via TargetScan and a luciferase reporter assessment. Rescue experiments were performed to uncover PICALM's involvement in miR-142-3p regulation during ischemic injury. In the presence of OGDR, miR-142-3p overexpression significantly promoted PI3K/Akt pathway activation, but this was mitigated by PICALM overexpression. Overall, miR-142-3p might provide neuroprotective benefits during OGDR injury by affecting PICALM and stimulating PI3K/Akt signaling, rendering it a possible therapeutic CIRI target.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143871261","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":"Editorial: A Child with ADNP Syndrome: A Case Study of Symptoms, Diagnostic Process and Innovative Behavioral Intervention Modes","authors":"Miroslav Holec,&nbsp;Illana Gozes","doi":"10.1007/s12031-025-02344-5","DOIUrl":"10.1007/s12031-025-02344-5","url":null,"abstract":"","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143871260","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}