Brain Research最新文献

{"title":"USP2 alleviates MPP+-induced neuronal injury by stabilizing FOXC1 in SK-N-SH cells","authors":"Zhijiang Zhuang ,&nbsp;Lihong Zhang ,&nbsp;Yizhao Wang","doi":"10.1016/j.brainres.2025.149689","DOIUrl":"10.1016/j.brainres.2025.149689","url":null,"abstract":"<div><h3>Background</h3><div>Forkhead box transcription factors play a crucial role in the development of various organ systems, and exhibit neuroprotective properties in many neurodegenerative diseases, including Parkinson’s disease (PD). However, the role and mechanism of Forkhead box C1 (FOXC1) in the pathogenesis of PD is poorly defined.</div></div><div><h3>Methods</h3><div>Human neuroblastoma SK-N-SH cells were treated with 1-methyl-4-phenylpyridinium (MPP⁺) to establish an <em>in vitro</em> model of PD. FOXC1 and Ubiquitin-specific peptidase 2 (USP2) mRNA levels were detected using real-time quantitative polymerase chain reaction (RT-qPCR). FOXC1, B-cell lymphoma-2 (Bcl-2), Bcl-2 related X protein (Bax), Cleaved caspase-3, and USP2 protein levels were determined using Western blot. Cell viability and apoptosis were analyzed using CCK-8 assay and flow cytometry. Tumor necrosis factor α (TNF-α), Interleukin-1β (IL-1β), and IL-6 levels were analyzed using ELISA. Reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and Glutathione (GSH) products were examined using special assay kits. After Ubibrowser online database prediction, the interaction between USP2 and FOXC1 was verified using Co-immunoprecipitation (CoIP) assay.</div></div><div><h3>Results</h3><div>FOXC1 and USP2 expression were decreased in PD patients and MPP⁺-treated SK-N-SH cells. MPP⁺ treatment could elicit SK-N-SH cell viability inhibition, inflammatory response, oxidative stress, and apoptosis promotion <em>in vitro</em>. Furthermore, overexpressing FOXC1 relieved MPP⁺-induced SK-N-SH cell injury <em>in vitro</em>. Mechanistically, USP2 directly interacted with FOXC1 and deubiquitinated FOXC1, therefore enhancing FOXC1 protein stability.</div></div><div><h3>Conclusion</h3><div>USP2 attenuated MPP⁺-triggered SK-N-SH cell injury through stabilizing FOXC1, providing a promising therapeutic target for PD treatment.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1862 ","pages":"Article 149689"},"PeriodicalIF":2.7,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143977066","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":"Neuroprotective potential of epigallocatechin gallate in Neurodegenerative Diseases: Insights into molecular mechanisms and clinical Relevance","authors":"Md. Al Amin ,&nbsp;Mehrukh Zehravi ,&nbsp;Sherouk Hussein Sweilam ,&nbsp;Mst Maharunnasa Shatu ,&nbsp;Trupti Pratik Durgawale ,&nbsp;Mohammad Shamim Qureshi ,&nbsp;Sumit Durgapal ,&nbsp;M. Akiful Haque ,&nbsp;Rajeshwar Vodeti ,&nbsp;Uttam Prasad Panigrahy ,&nbsp;Irfan Ahmad ,&nbsp;Sharuk L Khan ,&nbsp;Talha Bin Emran","doi":"10.1016/j.brainres.2025.149693","DOIUrl":"10.1016/j.brainres.2025.149693","url":null,"abstract":"<div><div>Neurodegenerative diseases (NDs) such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis pose significant challenges due to their complex pathophysiology and lack of effective treatments. Green tea, rich in the epigallocatechin gallate (EGCG) polyphenolic component, has demonstrated potential as a neuroprotective agent with numerous medicinal applications. EGCG effectively reduces tau and Aβ aggregation in ND models, promotes autophagy, and targets key signaling pathways like Nrf2-ARE, NF-κB, and MAPK. This review explores the molecular processes that underlie EGCG’s neuroprotective properties, including its ability to regulate mitochondrial dysfunction, oxidative stress, neuroinflammation, and protein misfolding. Clinical research indicates that EGCG may enhance cognitive and motor abilities, potentially inhibiting disease progression despite absorption and dose optimization limitations. The substance has been proven to slow the amyloidogenic process, prevent protein aggregation, decrease amyloid cytotoxicity, inhibit fibrillogenesis, and restructure fibrils for synergistic therapeutic effects. The review highlights the potential of EGCG as a natural, multi-targeted strategy for NDs but emphasizes the need for further clinical trials to enhance its therapeutic efficacy.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1860 ","pages":"Article 149693"},"PeriodicalIF":2.7,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143943703","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":"Landscape of spatial disruption of homeostasis in the middle temporal gyrus of epileptic patients","authors":"Lijian Han ,&nbsp;Jianping Liu ,&nbsp;Yuanying Song ,&nbsp;Sufang Wang ,&nbsp;Zevar Zeng ,&nbsp;Haicun Shi","doi":"10.1016/j.brainres.2025.149688","DOIUrl":"10.1016/j.brainres.2025.149688","url":null,"abstract":"<div><div>Epilepsy, a prevalent neurological disorder, significantly impacts cognitive function and quality of life, yet its underlying mechanisms remain incompletely understood. This study investigates the middle temporal gyrus (MTG) in epileptic patients using single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST) to elucidate cellular and spatial disruptions associated with epilepsy. We identified distinct cellular clusters and layer-specific gene expression patterns that were significantly altered in epileptic patients compared to controls. Notably, L5_6-related neurons increased, and L2_4-related neurons decreased in epilepsy, highlighting a reorganization of neuronal networks. Spatial mapping revealed significant alterations in the spatial domains of key marker genes, including NPY and GFAP, particularly in L5_6 layers. Using the spatial transition tensor (STT) algorithm, we characterized the spatial dynamics and multistability of neuronal populations, identifying regions of spatial stability and instability. NPY and GFAP emerged as critical genes linked to spatial homeostasis disruption. Additionally, specific L5_6 cell subtypes, such as those expressing TMSB10 and RPS23, exhibited significant spatial homeostasis disruption in epilepsy. These findings underscore the importance of integrating single-cell and spatial transcriptomic data to map cellular and spatial changes at high resolution, providing a comprehensive understanding of the interactions between cell types and their microenvironments. This study enhances our understanding of the molecular and cellular underpinnings of epilepsy and identifies potential therapeutic targets for restoring spatial stability and neuronal function in the epileptic brain.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1860 ","pages":"Article 149688"},"PeriodicalIF":2.7,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143936201","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 Targeting of Autosomal Parkinson’s Disease by Modulation of Leucine-Rich Repeat Kinase 2 (LRRK2) Protein","authors":"Zeeshan Hyderi ,&nbsp;Shirin Farhana M ,&nbsp;Tej Pal Singh ,&nbsp;Arumugam Veera Ravi","doi":"10.1016/j.brainres.2025.149674","DOIUrl":"10.1016/j.brainres.2025.149674","url":null,"abstract":"<div><div>Leucine-Rich Repeat Kinase 2 (LRRK2) is gaining attention as a key therapeutic target for autosomal dominant Parkinson’s disease (PD). The primary genetic aetiology of familial PD, accounting for around 5–6 % of familial cases and 2 % of sporadic cases, is mutations in the LRRK2 gene. The most prevalent mutation, G2019S, increases kinase activity, which phosphorylates important serine residues that control LRRK2 function, such as Ser910 and Ser935, leading to the development of PD. The development of LRRK2 inhibitors has emerged as a key area of study for PD therapy. In preclinical research, these inhibitors have demonstrated promise in reducing PD-related damage by altering the cellular localisation of LRRK2 and reduced phosphorylation. In addition to kinase action, LRRK2 is involved in autophagy and mitochondrial function. This participation implies that PD markers including mitochondrial dysfunction and defective autophagy may be addressed by LRRK2-targeted treatments. Moreover, selective LRRK2 inhibitors show promise in the treatment of PD, and more research into the molecular role of LRRK2 in PD is essential to developing efficient therapies that will improve patient outcomes and reduce the course of the illness. This review discusses the role of LRRK2 in pathogenesis of PD and current treatment approaches, particularly LRRK2 kinase inhibitors, and their potential to slow disease progression, along with recent advancements in clinical trials and future outlooks for improving outcomes in PD.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1860 ","pages":"Article 149674"},"PeriodicalIF":2.7,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143936198","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":"Neural mechanisms linking sleep disturbances to motor and cognitive impairments in Parkinson’s disease: Evidence from resting-state and task-based fNIRS","authors":"Hai-Yang Wang ,&nbsp;Zhanhua Liang ,&nbsp;Zhongrui Yan ,&nbsp;Yiming Liu","doi":"10.1016/j.brainres.2025.149681","DOIUrl":"10.1016/j.brainres.2025.149681","url":null,"abstract":"<div><h3>Background</h3><div>Sleep disturbances are common non-motor symptoms of Parkinson’s disease (PD), negatively affecting daily functioning, exacerbating motor symptoms, and contributing to cognitive impairment. However, the underlying neurobiological mechanisms are not well understood. This study utilized resting-state and task-based functional near-infrared spectroscopy (fNIRS) to explore how sleep disturbances affect brain function in PD patients at the neural level.</div></div><div><h3>Methods</h3><div>Sixty PD patients were recruited, including 30 with sleep disturbances and 30 without. Resting-state fNIRS and clinical assessments were used to analyze spontaneous brain activity and functional connectivity. We also examined the mediating role of brain activity in the relationship between sleep disturbances and motor symptoms. The verbal fluency test (VFT) was employed to investigate changes in brain mechanisms related to executive function in patients with sleep disturbances.</div></div><div><h3>Results</h3><div>Resting-state analysis revealed significantly increased fractional amplitude of low-frequency fluctuations (fALFF) in the medial prefrontal cortex (mPFC) in PD patients with sleep disturbances. fALFF values were negatively correlated with sleep quality and positively with motor symptom severity. Mediation analysis indicated that spontaneous neural activity in the mPFC partially mediated the relationship between sleep disturbances and motor symptoms. Task-based analysis showed reduced activation in the mPFC and orbitofrontal cortex (OFC) during the VFT in patients with sleep disturbances, indicating impaired executive function.</div></div><div><h3>Conclusion</h3><div>Sleep disturbances in PD could be associated with exacerbated motor symptoms and may impair executive function by affecting spontaneous and task-related neural activity in the mPFC. These findings highlight mPFC dysfunction as a potential biomarker for targeted therapies.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1860 ","pages":"Article 149681"},"PeriodicalIF":2.7,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143936199","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":"Phenotypic plasticity: historical context, theories and DOHaD","authors":"Joaci Pereira dos Santos Júnior ,&nbsp;Osmar Henrique dos Santos Júnior ,&nbsp;Eulália Rebeca Silva-Araujo ,&nbsp;Henrique José Cavalcanti Bezerra Gouveia ,&nbsp;Diego Cabral Lacerda ,&nbsp;Diego Bulcão Visco ,&nbsp;Paula Brielle Pontes Silva ,&nbsp;Erika Vanessa Cadena-Burbano ,&nbsp;Isla Ariadny Amaral de Souza Gonzaga Paz ,&nbsp;Sandra Lopes de Souza ,&nbsp;Raul Manhães de Castro","doi":"10.1016/j.brainres.2025.149673","DOIUrl":"10.1016/j.brainres.2025.149673","url":null,"abstract":"<div><div>The Developmental Origins of Health and Disease (DOHaD) concept has emerged as an interdisciplinary framework that explores how early-life events shape long-term health and disease risk. Rooted in the Thrifty Phenotype hypothesis proposed by Barker and Hales, DOHaD builds upon centuries of philosophical and scientific thought. Central to DOHaD is the concept of phenotypic plasticity, which explains how organisms adapt their biological characteristics in response to environmental stimuli, particularly during critical developmental periods. In this context, this review aims to analyze the historical evolution of phenotypic plasticity, its theoretical foundations, and its role in health and disease. After reviewing the literature on scope, we summarize key contributions from evolutionary biology, genetics, and epigenetics, examining theories from Lamarck, Darwin, Mendel, and Waddington to contemporary perspectives in DOHaD. Understanding that early-life events can lead to adaptations which may have short-term benefits but potentially increase the likelihood of diseases in adulthood highlights the importance of targeted preventive interventions. Additionally, individual variations in response to environmental stimuli reinforce the complexity of adaptive mechanisms. Thus, understanding the intricate relationship between phenotypic plasticity, early-life exposures, and disease risk is essential for developing preventive interventions and public health strategies. The challenge remains in translating these findings into effective healthcare policies and clinical applications, ensuring improved quality of life and disease prevention across generations.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1860 ","pages":"Article 149673"},"PeriodicalIF":2.7,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143928072","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":"Mitochonic acid 5, an ATP production accelerator, protects against neurological damage in ischemic stroke","authors":"Shinomi Sasaibe,&nbsp;Yukie Yoshioka,&nbsp;Yoshiki Kuse,&nbsp;Shinsuke Nakamura,&nbsp;Masamitsu Shimazawa","doi":"10.1016/j.brainres.2025.149664","DOIUrl":"10.1016/j.brainres.2025.149664","url":null,"abstract":"<div><div>Cerebral infarction is a severe condition that causes motor dysfunction and disorientation due to irreversible neuronal cell death. After an ischemic stroke, the lack of oxygen and nutrients induces cerebral neuronal damage along with mitochondrial dysfunction. Therefore, activating mitochondrial function is a promising strategy for treating ischemic stroke. This study aimed to examine whether Mitochonic acid 5 (MA-5), a compound that targets mitochondria to stimulate ATP synthesis, has protective effects against cerebral ischemia/reperfusion (I/R) injury. We first confirmed that MA-5 significantly increases ATP production after 1 h of exposure to neuron-like cells. MA-5 also increased ATP production coupled respiration in SH-SY5Y cells after the induction of OGD/R. After inducing cerebral I/R in mice via transient midbrain occlusion (t-MCAO), the administration of MA-5 reduced neurological deficits and infarct volume. In addition, MA-5 suppressed the increase in the Bax/Bcl-2 ratio, an index of mitochondria-mediated apoptosis after t-MCAO. Taken together, these results suggest that MA-5 may be a useful therapeutic agent against ischemic stroke by activating mitochondrial function.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1860 ","pages":"Article 149664"},"PeriodicalIF":2.7,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143923492","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 multi-channel implantable micro-magnetic stimulator for synergistic magnetic neuromodulation","authors":"Lei Dong ,&nbsp;Yenan Qi ,&nbsp;Mengying Luan ,&nbsp;Qiwen Liu ,&nbsp;Meng Wang ,&nbsp;Chunxiao Tian ,&nbsp;Yu Zheng","doi":"10.1016/j.brainres.2025.149679","DOIUrl":"10.1016/j.brainres.2025.149679","url":null,"abstract":"<div><div>Micro-magnetic stimulation (μMS) is an emerging technology in magnetic neuromodulation. However, for larger brain structures with complex neural pathways, such as deep brain neural clusters, traditional implantable single-point μMS devices are immobile and incapable of multi-regional magnetic modulation. While multi-channel μMS can effectively address this limitation, its large size, difficulty in implantation, and unclear synergistic modulation patterns restrict its application. To tackle these challenges, this study designs a 4 × 4 array micro-coil structure targeted at the deep hippocampal region of the mouse brain. Numerical simulations were performed to analyze the coupling coefficients among the micro-coils and the distribution of the electromagnetic field in the structure, indicating that, with optimized parameters, the effective magnetic stimulation threshold can be achieved. Based on this, a multi-channel μMS device was fabricated, solving key issues such as waterproofing, biocompatibility, and dual-brain-region implantation of both stimulation and recording electrodes. A multi-point synergistic magnetic stimulation protocol was developed. After determining the synergistic magnetic stimulation parameters and effective target positions through in vitro experiments, real-time monitoring of calcium signal changes in the CA1 region of the hippocampus in mice during synergistic magnetic stimulation was performed. The results demonstrate that synergistic magnetic stimulation significantly enhances synaptic plasticity and calcium signal activity. This validates the feasibility of the implantable multi-channel micro-magnetic stimulator.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1860 ","pages":"Article 149679"},"PeriodicalIF":2.7,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143924060","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":"Challenges and hopes for treatment of anxiety disorder in the autistic population","authors":"Tomasz Dulski ,&nbsp;Sanata Tolak ,&nbsp;Justyna Zmorzyńska","doi":"10.1016/j.brainres.2025.149675","DOIUrl":"10.1016/j.brainres.2025.149675","url":null,"abstract":"<div><div>Anxiety disorders, marked by excessive fear and worry, are particularly prevalent in autism, affecting up to 45 % of individuals with the condition. Since the 1960s, advances in neuroscience, psychology, and psychopharmacology have enhanced understanding and treatment of anxiety disorders in general population. Standardized diagnostic criteria development facilitated accurate classification of anxiety disorders. Neurobiological research identified key brain regions forming the basis of the amygdala-centred fear circuit model. Pharmacological advancements introduced selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) as safer, first-line treatments. However, these medications show limited efficacy and significant side effects in autistic individuals, highlighting the need for alternative treatments. Cognitive-behavioural therapy (CBT) has gained empirical support, helping to reduce avoidance behaviours, but modifications are often needed for autistic individuals. Emerging therapies, including Mindfulness-Based Stress Reduction for Autism Spectrum Disorder (MASSI) and virtual reality-based interventions, are being explored for individuals with more treatment-resistant anxiety. Ongoing clinical trials are assessing medications used for other psychiatric disorders to determine their efficacy in anxiety treatment for autism. Recent genetic and neuroimaging research has revealed altered brain connectivity and genetic susceptibility in anxiety, promoting the development of personalized treatments. Despite these advances, challenges remain in optimizing interventions and addressing treatment resistance, necessitating continued research and innovation.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1860 ","pages":"Article 149675"},"PeriodicalIF":2.7,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143918415","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":"Gut microbiota mediated regulation of vitamin B homeostasis in autism spectrum disorders","authors":"Esma Karahmet Farhat ,&nbsp;Ines Banjari ,&nbsp;Amina Džidić-Krivić ,&nbsp;Malik Ejubović ,&nbsp;Emina Karahmet Sher","doi":"10.1016/j.brainres.2025.149661","DOIUrl":"10.1016/j.brainres.2025.149661","url":null,"abstract":"<div><div>The exact cause of autism spectrum disorder (ASD) is yet unknown, although possible causes include early childhood, foetal development, gestation, delivery mode, genetics, and environmental variables. Approximately 1% of children worldwide have ASD, and this percentage is rising. The immunological, endocrine, gut microbiota and brain-gut axis quality influence the intensity of ASD symptoms. Deficits in the composition and diversity of gut microbiota are common in children with ASD, accounting for 9–90% of these illnesses, including elevated inflammatory cytokines, inflammation, leaky gut syndrome, and pathological microflora growth. Dysbiosis can be made worse by eating issues that are prevalent in ASD. B vitamins, such as cobalamin and folate, which are essential methyl donors for DNA epigenetic changes, are usually produced by a healthy gut microbiota. 50% of people with ASD have a vitamin B deficit. This work summarises research on the impact of gut microbiota on DNA methylation and B vitamin synthesis in ASD, as well as etiological variables connected to dysbiosis. Probiotics, postbiotics, and vitamin B therapies in kids with ASD should be investigated in future studies.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1860 ","pages":"Article 149661"},"PeriodicalIF":2.7,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143918127","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}