Neurotoxicity Research最新文献

{"title":"Therapeutic Effects of miR-29b-Enriched Nanovesicles on Mitochondrial Injury and Neuroinflammatory Processes in Alzheimer's Disease.","authors":"Sinan Gönüllü, Elif Dalkılınç, Oğuz Çelik, Hamit Çelik, Sefa Küçükler, Ahmet Topal, Ramazan Akay, Mustafa Onur Yıldız, Bülent Alım, Selçuk Özdemir","doi":"10.1007/s12640-026-00823-0","DOIUrl":"10.1007/s12640-026-00823-0","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is defined by the accumulation of extracellular amyloid-β plaques and intracellular neurofibrillary tangles, which drive neuronal and synaptic impairment. In AD, the accumulation of protein aggregates leads to neuroinflammation, increased oxidative stress, and mitochondrial damage, resulting in neuronal loss and cognitive impairment. Emerging evidence highlights that microRNAs (miRNAs) modulate AD-related pathological pathways and may offer opportunities for therapeutic intervention. In this study, we investigated the therapeutic potential of microRNA-29b (miR-29b) delivered via small extracellular vesicles (sEVs) in an in vitro neuroblastoma model of AD. Four experimental groups were established using SH-SY5Y neuroblastoma cells: (1) untreated control cells, (2) Aβ-treated cells to model AD-like pathology, (3) cells treated with unloaded sEVs, and (4) cells treated with miR-29b-loaded sEVs (sEV-miR-29b). To evaluate treatment effects, we assessed markers of oxidative stress (ROS, LDH, SOD, MDA, GPX1), neuroinflammation (BDNF, ICAM1, TNF-α, NfL, MIF, VEGFA, MCP-1), mitochondrial dysfunction (Cytc, TFAM, PINK1, DNM1L), synaptic integrity (CPLX2, ROR1), and AD pathology (Amyloid-β, Total Tau, pTau181, pTau217). Our findings demonstrate that treatment with sEV-miR-29b attenuated Aβ-induced oxidative stress, reduced pro-inflammatory signaling, and improved mitochondrial homeostasis compared with Aβ-only and sEV-only groups. Moreover, sEV-miR-29b treatment partially restored synaptic protein expression and decreased pathological tau phosphorylation. These results indicate that miR-29b plays a regulatory role in neuroinflammation, oxidative stress, and mitochondrial function, suggesting that sEV-mediated delivery of miR-29b represents a promising therapeutic strategy for modulating AD-related neurodegenerative mechanisms. This study highlights the potential of miR-29b-loaded sEVs as a therapeutic approach for AD.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"44 5","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148813623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding the Neuroinflammatory Potential of Non-Nutritive Sweeteners Through An Integrative Computational Approach.","authors":"Shreya Chakraborty, Venkatraman Manickam","doi":"10.1007/s12640-026-00822-1","DOIUrl":"10.1007/s12640-026-00822-1","url":null,"abstract":"<p><p>Non-nutritive sweeteners (NNS) are commonly used in the beverage, food, and pharmaceutical industries, however, their possible link to neuroinflammation remains a contentious issue. Hence, to investigate this potential association and identify the molecular pathways involved, targets of the most frequently consumed NNSs, namely sucralose, aspartame, acesulfame, cyclamate, and saccharin, were extracted from the STITCH, Super-PRED, STP, SEA and CTD databases, while neuroinflammatory targets were extracted from GeneCards, OMIM, and NCBI databases. A total of 124 targets were obtained by overlapping NNS and neuroinflammatory targets, of which 20 key targets, including CASP3, PPARγ, MTOR, and MMP9, were identified for further analysis. KEGG enrichment analysis suggested a significant association of these targets with pathways related to Alzheimer's disease and neuroactive ligand-receptor interaction. Gene Ontology analysis revealed enrichment in biological processes associated with inflammatory response and reactive oxygen species. The associated cellular components were primarily localised in the axon, dendrite, and synaptic membrane. Molecular docking followed by molecular dynamics simulations was performed to evaluate the stability of the NNS-key target complexes, revealing favourable binding affinities and stable interaction profiles. Gene expression analysis of these key targets predicted their differential regulation across four majorly recognised neuroinflammatory disorders, including Alzheimer's disease, multiple sclerosis, Parkinson's disease, and amyotrophic lateral sclerosis, with a significant up or downregulation of these key targets. Results of this study suggest that NNS may be associated with neuroinflammatory processes through these key targets and identified pathways, highlighting the need for improving the standards in food safety.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"44 5","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148813594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal Exposure to Anxiolytics: A Critical Review on Brain Development and Neurobehavioral Manifestations in Offspring.","authors":"K P Singh, Anamika Dubey","doi":"10.1007/s12640-026-00820-3","DOIUrl":"10.1007/s12640-026-00820-3","url":null,"abstract":"<p><p>Anxiety disorders are among the most common mental health conditions affecting women of reproductive age, and a significant proportion of pregnant women experience clinically relevant anxiety symptoms. In some cases, pharmacological treatment may be required to manage severe or persistent symptoms; however, concerns remain regarding the potential impact of prenatal exposure to anxiolytic medications on fetal brain development. The developing nervous system undergoes critical processes during gestation, including neuronal proliferation, migration, and synaptic formation, which may be sensitive to pharmacological influences. This review examines available clinical and preclinical evidence regarding the neurodevelopmental consequences of prenatal exposure to commonly used anxiolytic medications, especially benzodiazepines (BZDs) and azapirones (AZPs). Evidence from observational human studies has shown associations between prenatal exposure to BZDs and certain neonatal and neurodevelopmental outcomes. However, results remain inconsistent and may be influenced by confounding factors, including maternal psychiatric conditions, co-medication use, and environmental variables. In contrast, data on prenatal exposure to AZPs, especially buspirone, are relatively limited, with most of the available evidence coming from small cohorts and preclinical models. Experimental studies provide mechanistic insights suggesting that early-life exposure to anxiolytic agents may influence neurotransmitter systems, neuronal morphology, and behavioral development in offspring. However, translating findings from animal models to the human clinical context remains challenging. Overall, the current literature highlights substantial knowledge gaps regarding dose-dependent effects, critical developmental windows, and long-term neurobehavioral outcomes. Further well-controlled longitudinal and translational studies are needed to clarify the potential implications of prenatal exposure and to support evidence-based clinical decision-making during pregnancy.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"44 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148766350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oral Administration of Different Forms of Exogenous Tau Protein Induces Multi-Organ Defects Across Developmental Stages in Drosophila melanogaster.","authors":"Surajita Sahu, Hariharakrishnan Chidamabaram, Vaishnavi Ananthanarayanan, Tazeen Qureshi, SmitaEknath Desale, Madhura Chandrashekar, Rashmi Santhoshkumar, Monalisa Mishra, Subashchandrabose Chinnathambi","doi":"10.1007/s12640-026-00818-x","DOIUrl":"10.1007/s12640-026-00818-x","url":null,"abstract":"<p><p>Tau is a crucial protein involved in many neurodegenerative diseases, including Alzheimer's disease. Natively, Tau is an unfolded protein found predominantly in axons that play a vital role in maintaining and stabilizing microtubules. Under pathological circumstances, Tau disengages from microtubules and forms insoluble intracellular filaments on its own, building neurofibrillary tangles in the brains of Alzheimer's patients. Although Tau exists in aggregates found in the brain and gut of Alzheimer's patients, the function of Tau in the brain is well studied, while the role of Tau in the gut needs further investigation. We have investigated the effects of Tau monomer, oligomer, and aggregates at 10 µM concentration via feeding them to the third instar larvae. To evaluate the genotoxicity, we did 4', 6-diamidino-2-phenylindole staining, while dichloro-dihydro-fluorescein diacetate staining was performed to assess cytotoxicity. Furthermore, we performed a TUNEL assay to detect apoptotic cells. Additionally, we carry out an NBT assay for biochemical estimation of reactive oxygen species by extracting hemolymph. Phenotypes were examined in different stages, i.e., larvae, pupae, and adult flies. Histological studies were performed on eye, gut tissue and reproductive organs of D. melanogaster to check the cytoskeletal alterations. The current study finds that the administration of monomer, oligomer, and aggregate forms causes genotoxicity, cytotoxicity, and cytoskeletal defects in D. melanogaster.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"44 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148723549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metformin Enhances Antioxidant Defenses and Limits Lipid Peroxidation Through the Modulation of Nrf2/KEAP1 Pathway in Hippocampal Neurons Exposed to Amyloid-β Oligomers.","authors":"Jorge Arriagada, Matías Lantadilla, Pedro Lobos, Adolfo A Paz, Emilio A Herrera, Pablo Muñoz, Andrea Paula-Lima","doi":"10.1007/s12640-026-00819-w","DOIUrl":"10.1007/s12640-026-00819-w","url":null,"abstract":"<p><p>Oxidative stress is an early and important feature of Alzheimer's disease (AD) that contributes to synaptic dysfunction and neurodegeneration. Soluble amyloid-β oligomers (AβOs) are major contributors to oxidative damage and have been shown to impair neuronal antioxidant defenses. The Nrf2/KEAP1 pathway is a central regulator of cellular redox homeostasis; however, its activity is compromised in AD, increasing neuronal vulnerability to oxidative stress. Metformin (Met), a widely used antidiabetic drug, has emerged as a potential modulator of antioxidant signaling pathways in the nervous system. In the present study, we investigated whether Met enhances antioxidant defenses in primary fetal rat hippocampal neurons exposed to AβOs. Neuronal cultures were treated with Met (2.5 mM for 24 h) prior to exposure to AβOs (500 nM for 6 h). We evaluated Nrf2 and KEAP1 protein levels, Nrf2 nuclear localization, antioxidant enzyme expression and activity, and lipid peroxidation. Met treatment promoted Nrf2 nuclear accumulation, preserved a favorable Nrf2/KEAP1 profile under amyloid stress, and enhanced the expression and activity of key antioxidant enzymes, including superoxide dismutase (SOD1 and SOD2), catalase (CAT), and glutathione peroxidase (GPx1/2). In addition, Met attenuated AβOs-induced lipid peroxidation, supporting its protective effects against amyloid-associated oxidative damage. Collectively, these findings indicate that Met strengthens neuronal antioxidant defenses and promotes redox resilience under amyloid-associated oxidative stress. Our results support modulation of the Nrf2/KEAP1 pathway as a mechanism contributing to the neuroprotective actions of Met and identify the coordinated enhancement of antioxidant defenses and reduction of lipid peroxidation as key components of neuronal redox resilience against AβOs-induced stress.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"44 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148723277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal Coca Paste Exposure Impairs Hippocampal Neuronal Development and Recognition Memory in Offspring.","authors":"Vanina Clouzet, Alberto Rafael, Andrea Cairus, Giuliana Gonzalez, Marcela Martínez, José Pedro Prieto, Nathalia Vitureira","doi":"10.1007/s12640-026-00817-y","DOIUrl":"10.1007/s12640-026-00817-y","url":null,"abstract":"<p><p>Illicit psychostimulant use during pregnancy represents a major public health issue due to its detrimental effects on offspring neurodevelopment. Prenatal exposure to smokable cocaine derivatives such as crack cocaine and coca paste (CP) is particularly concerning, as it has been associated with an increased risk of impairments in learning, memory, and social behavior from birth through early childhood. CP's low cost, wide availability, high toxicity, and strong addictive potential heighten its danger. While CP use during pregnancy is well documented, its specific neurodevelopmental consequences remain poorly understood compared to those of crack. Here, we used a rat model to examine the effects of chronic prenatal exposure to a street-grade CP sample obtained from police seizures on hippocampal neuronal morphogenesis, synaptogenesis, and function, as well as hippocampus-dependent recognition memory. Primary hippocampal neurons from neonates prenatally exposed to CP once daily from gestational day (GD) 8 until GD21 showed reduced neuronal survival, impaired neurite outgrowth, and decreased dendritic complexity, together with reduced synaptic vGlut1 abundance. These structural alterations were accompanied by significant deficits in recognition memory in the novel object recognition task in juvenile offspring. Our findings suggest that prenatal CP exposure disrupts hippocampal development and function, leading to cognitive deficits. This study supports the severe neurodevelopmental risks associated with prenatal CP exposure and underscores the importance of preventive strategies addressing drug use during pregnancy.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"44 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148685334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of an Integrated In Silico-In Vitro Pipeline for Predicting Mitochondrial Complex I-Mediated Neurotoxicity of Chlorpyrifos.","authors":"Fuat Karakuş, Muhammed Tilahun Muhammed, Ege Arzuk","doi":"10.1007/s12640-026-00816-z","DOIUrl":"10.1007/s12640-026-00816-z","url":null,"abstract":"<p><p>Chlorpyrifos (CPF) is a broad-spectrum chlorinated organophosphate insecticide. It was classified as a persistent organic pollutant under the Stockholm Convention in 2024 due to its harmful effects on the environment and human health, including neurotoxicity. The classical mechanism of CPF-induced neurotoxicity is attributed to acetylcholinesterase inhibition by its metabolite, chlorpyrifos-oxon (CPO), in cholinergic neurons. Emerging studies indicate that CPF also induces toxicity in dopaminergic neurons through mitochondrial dysfunction. In this study, the molecular mechanisms and targets associated with CPF-induced neurotoxicity in humans were investigated using network toxicology, molecular docking, molecular dynamics, and in vitro study. Comprehensive database analyses identified 271 potential targets associated with CPF-induced neurotoxicity. Gene ontology enrichment and gene-gene interaction analyses revealed significant enrichment related to mitochondria and oxidative phosphorylation. Protein-protein interaction and centrality analyses identified 15 hub targets. Molecular docking and molecular dynamics simulations demonstrated that CPF and CPO bind to mitochondrial Complex I, especially with NDUFA2, more strongly than rotenone, a known Complex I inhibitor. In vitro analysis in SH-SY5Y cells demonstrated that CPF impaired mitochondrial complex I-associated activity in a concentration-dependent manner, with significant inhibition observed at concentrations of 75 µM and higher. These findings suggest that CPF, and to a lesser extent CPO, may exert inhibitory effects on mitochondrial complex I in neurons, thereby contributing to neurotoxicity in humans. Overall, these results are in line with previous experimental reports and highlight the effectiveness of integrated computational approaches in identifying key mitochondrial mechanisms involved in CPF-induced neurotoxicity.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"44 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148679586","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of Glutamate Decarboxylase in the Spinal Cord Induces Motor Deficits and Motor Neuron Degeneration.","authors":"Elizabeth Colín-Martínez, Uri Nimrod Ramírez-Jarquín, Ricardo Tapia, Clorinda Arias","doi":"10.1007/s12640-026-00815-0","DOIUrl":"10.1007/s12640-026-00815-0","url":null,"abstract":"<p><p>Motor neuron (MN) diseases such as amyotrophic lateral sclerosis (ALS) are characterized by the loss of cortical and spinal MNs. Although the precise mechanisms of MN degeneration are still unknown, downregulation of GABAergic circuits has been identified in both ALS patients and transgenic models of the disease. GABA synthesis depends on the activity of the enzyme glutamate decarboxylase (GAD), of which two isoforms are known: GAD65 and GAD67. To study the effects of decreased GABA synthesis on spinal cord motor function, we analyzed the effects of administering three selective inhibitors of GAD: 3-mercaptopropionic acid (MPA), a competitive inhibitor of GAD, thiosemicarbazide (TSC), and pyridoxal phosphate γ-glutamyl hydrazone (PLPGH), two GAD cofactor blockers. A single dose of any of these inhibitors did not affect motor behavior or MN morphology. However, subchronic (3 days) and chronic (10 days) administration of MPA, TSC or PLPGH in rats caused motor alterations and cellular changes, including episodic myoclonus-like movements, flaccidity in the ipsilateral phalanges, loss of 35-50% of MNs, reactive astrogliosis and decreased GAD activity. These findings suggest that chronic inhibition of GAD can lead to MN degeneration and further suggest that GABA metabolism in the spinal cord may participate in the mechanisms that cause MN death in patients with neurodegenerative diseases such as ALS.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"44 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13442598/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148679550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: C-terminal Domain of the Heavy Chain of Tetanus Toxin Ameliorate Lipopolysaccharide Induced Hemiparkinsonism in Rats.","authors":"Irving Parra, José Aguilera, Yousef Tizabi, Liliana Mendieta","doi":"10.1007/s12640-026-00814-1","DOIUrl":"10.1007/s12640-026-00814-1","url":null,"abstract":"","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"44 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13421188/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Melatonin Modulates Behavioral and Physiological Responses in a Concentration-dependent Manner in a Pilocarpine-induced Seizure-like Model Using Zebrafish Larvae.","authors":"Lorrânny Pereira de Assis Valadares, Bianca Leite Carnib, Bruno Dos Santos Ferreira Roque, Felipe Cirqueira, Thiago Lopes Rocha, Mônica Rodrigues Ferreira Machado, Marina Pacheco Miguel","doi":"10.1007/s12640-026-00812-3","DOIUrl":"10.1007/s12640-026-00812-3","url":null,"abstract":"<p><p>Melatonin has been extensively studied for its antioxidant activity, yet its safety profile and concentration-dependent effects remain only partially understood, particularly in aquatic experimental systems. Here, we investigated the effects of melatonin on behavioral and physiological responses in a pilocarpine (PILO)-induced seizure-like model using zebrafish (Danio rerio) larvae. A multibiomarker framework was employed, combining embryo-larval toxicity assessments up to 144 h post-fertilization with behavioral and biochemical endpoints related to seizure-like activity. Across the tested concentration range (0.14-18 µg/mL), melatonin did not affect mortality or hatching rates. However, exposure to higher concentrations (9.0 and 18 µg/mL) resulted in altered spontaneous contractions and increased embryonic heart rate, indicating measurable physiological changes during early development. At lower concentrations (2.25 and 4.50 µg/mL), melatonin was associated with reduced PILO-induced hyperlocomotion, increased latency to seizure-like onset, and reduced progression to more severe behavioral stages. These responses were accompanied by a reduction in reactive oxygen species (ROS) levels at both 72 and 144 hpf. Collectively, the data reveal a concentration-dependent response profile, with distinct behavioral and physiological outcomes emerging across exposure levels. This study contributes to the characterization of melatonin effects in zebrafish larvae and underscores the importance of dose selection in experimental seizure models.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"44 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13396114/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148579533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}