Neurochemical Research最新文献

{"title":"Circadian Rhythm Cascade SIRT1/PGC-1α/BMAL1 Pathway Regulates Nitroglycerin-Induced Chronic Migraine","authors":"Wei Liu,&nbsp;Zhebin Liu,&nbsp;Hongli Dong,&nbsp;Zhengxin Ni,&nbsp;Yuanyi Wang,&nbsp;Yunjuan Li,&nbsp;Huifeng Qian,&nbsp;Yue Hu,&nbsp;Yu Zuo","doi":"10.1007/s11064-025-04513-9","DOIUrl":"10.1007/s11064-025-04513-9","url":null,"abstract":"<div><p>Previous findings have suggested that inflammation activation in the trigeminal nervous system and circadian rhythms disruption contributed to the chronic migraine (CM). Linking the two critical processes, the involvement of signaling cascade SIRT1/PGC-1α/BMAL1 in CM is suggested. Our objective is to elucidate the important signaling cascade implicated in the CM pathogenesis, hence enhancing the comprehension of the mechanisms underlying CM development. NTG-induced migraine model was established. Thresholds of thermal and mechanical stimulation were examined in sensory sensitivity test, and western blot (WB) of CGRP and c-Fos evaluated CM severity. Co-immunoprecipitation (CoIP) assessed SIRT1 and PGC-1<i>α</i> interaction, while chromatin immunoprecipitation quantitative PCR (ChIP-qPCR) examined their binding rates to the BMAL1 promoter. Additionally, cell transfection and SRT1720 administration were performed to further investigate the regulatory role of the pathway. In the NTG-induced migraine model, inflammation activation and the aberrant expression of circadian rhythm-related genes and hormones were detected. The downregulation of SIRT1 and PGC-1<i>α</i> activity, along with the interactions within the pathway, provided evidence of this pathway plays a role in regulating migraine. The overexpression of SIRT1 through virus injection and SRT1720 administration both demonstrated the effect of alleviating the key link of CM mechanisms, including central sensitization and inflammatory activation in the trigeminal nucleus and circadian rhythms disruption. Moreover, the anti-inflammatory effect was further demonstrated to be mediated by BMAL1 by using shRNA.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144832300","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":"Longitudinal Brain Structural, Neurochemical, and Behavioral Changes Following Traumatic Brain Injury in Immature Rat Brain with ALCAR Treatment","authors":"Susanna Scafidi,&nbsp;Su Xu,&nbsp;Jennifer N. Jernberg,&nbsp;Tiffany Chu,&nbsp;Gary Fiskum,&nbsp;Mary C. McKenna","doi":"10.1007/s11064-025-04494-9","DOIUrl":"10.1007/s11064-025-04494-9","url":null,"abstract":"<div><p>Pediatric survivors of traumatic brain injury (TBI) suffer from long-term neurologic disabilities, including deficits in memory and learning. Proton magnetic resonance spectroscopy (¹H-MRS) can assess alterations in brain neurochemical profile non-invasively in vivo over time. Our study aimed to evaluate (1) the longitudinal metabolic alterations in the hippocampus after TBI using in vivo ¹H-MRS and MRI in developing rat brain, and (2) test whether treatment with acetyl-L-carnitine (ALCAR) affects hippocampal metabolic profile. Using a controlled cortical impact model of TBI, we used post-natal day (PND) 21 rat pups and acquired longitudinal ¹H-MRS of the ipsilateral perilesional and contralateral hippocampi 2–4 h, 24 h, 72 h, 7 days, and 21 days post injury. Behavioral analysis was performed on post-injury days (Dpi) 3–7, 14, and 21–28. ALCAR treated rats received intraperitoneal administration (100 mg/kg) at 1 h, 4 h, 12 h, and 23 h post injury. Our results show that TBI in immature brain results in long-term structural and neurochemical alterations. TBI resulted in long–term decreased hippocampal volume and a reduction in levels of glutamate (Glu), glutamine (Gln),γ-aminobutyric acid (GABA), myo-inositol (Ins) and taurine (Tau) in the ipsilateral (injured) hippocampus up to 72 h post injury. In TBI + vehicle and TBI + ALCAR groups, N-acetyl-aspartate (NAA) remained decreased 21 days post injury. Treatment with ALCAR did not significantly change hippocampal neurochemical profile at 24 h post injury. Behavioral studies in TBI-injured rats demonstrated that sensory motor function decreased initially and recovered with time. The TBI + ALCAR group performed significantly better compared to TBI + vehicle group in both sensory motor and hippocampal dependent recognition memory. Further studies with the longer duration of ALCAR administration are necessary to adequately assess the efficacy of ALCAR following pediatric TBI.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12310762/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144740804","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":"Chrysophanol Attenuates Cognitive Impairment, Neuroinflammation, and Oxidative Stress by TLR4/ NFκB-Nrf2/HO-1 Signaling in Ethanol-Induced Neurodegeneration","authors":"Jehan Zeb Khan,&nbsp;Syeda Rida Zainab,&nbsp;Abdullah Alattar,&nbsp;Reem Alshaman,&nbsp;Fawad Ali Shah,&nbsp;Muhammad Khalid Tipu","doi":"10.1007/s11064-025-04486-9","DOIUrl":"10.1007/s11064-025-04486-9","url":null,"abstract":"<div><p>Ethanol-induced neurodegeneration refers to the progressive loss of structure and function of neurons caused by chronic ethanol consumption. According to the World Health Organization (WHO), over 2.3 billion people globally consume alcohol. This contributes to a significant amount of alcohol-related brain damage. This study evaluated the effect of chrysophanol in ethanol-induced neurodegeneration. Mice were administered 10 mg/kg i.p. chrysophanol, 30 min after a 2 g/kg i.p. injection of ethanol, for 11 days. Y-maze, Morris water maze (MWM), and novel object recognition (NOR) test were carried out to analyze learning and memory impairment. Analysis of antioxidant levels, histopathological examinations, measurement of COX-2 &amp; NLRP3 using ELISA, and gene expression analysis of TLR4, NFκB, IL-1β, TNF-α, Caspase-3, and Nrf-2, HO-1, and in hippocampus and cortex using RT-PCR, as well as DNA damage by comet assay, were carried out. Chrysophanol has shown a remarkable impact in reversing cognitive decline and spatial memory. It effectively boosted antioxidant levels such as GSH, GST, and CAT, while simultaneously reducing the levels of MDA and NO. The histopathological analysis also showed improvement in overall morphology and survival of neurons. Chrysophanol treatment effectively showed an increase in the expression of HO-1 and Nrf-2, with a decrease in TLR4, NFκB, IL-1β, TNF-α, and Caspase-3 expression confirmed through RT-PCR. Production of inflammatory cytokines and apoptotic gene expression was successfully reversed after chrysophanol treatment. COX-2 &amp; NLRP3 levels decreased, and an improvement in DNA damage was observed after chrysophanol treatment. In conclusion, chrysophanol demonstrated remarkable neuroprotective activity against ethanol-induced neurodegeneration.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726409","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":"Orchestrating the Matrix: The Role of Glial Cells and Systemic Signals in Perineuronal Net Dynamics","authors":"Valentino Totaro,&nbsp;Tommaso Pizzorusso,&nbsp;Paola Tognini","doi":"10.1007/s11064-025-04506-8","DOIUrl":"10.1007/s11064-025-04506-8","url":null,"abstract":"<div><p>Perineuronal nets (PNNs) are specialized, dense extracellular matrix structures that enmesh the cell bodies and dendrites of specific neurons, most notably inhibitory interneurons. Increasing evidence indicates that PNNs serve not merely as passive scaffolds but play an active and essential role in modulating synaptic plasticity and circuit physiology. They critically influence the timing of sensory system critical periods, as well as processes underlying learning, memory, and higher cognitive functions. Furthermore, dysregulation of PNN density and architecture have been associated with conditions like autism, neurodevelopmental disorders, schizophrenia and Alzheimer’s disease. Since they are extensively involved in brain function, we discuss the multitude of regulatory factors that govern the formation, maturation, and remodeling of PNNs. In particular, we focus on both molecular and cellular brain-intrinsic mechanisms, highlighting the potential contributions of microglia and astrocyte derived factors. Additionally, we consider the influence of long-range signaling cues, including the metabolic status and peripheral hormones. Analysing this complex network of interactors, we try to highlight the role of PNNs beyond neural plasticity and brain function, in a broader whole-body physiological perspective.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12307546/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726412","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":"Candesartan Mitigates Perioperative Neurocognitive Disorders by Modulating Hypertension-Linked Neuroinflammatory Factor","authors":"Zhenyu Wu,&nbsp;Yuqing Li,&nbsp;Taowu Gong,&nbsp;Jia Li,&nbsp;Pengcheng Zhao,&nbsp;Xufang Huo,&nbsp;Yuhang Zhu,&nbsp;Qingfan Zeng","doi":"10.1007/s11064-025-04499-4","DOIUrl":"10.1007/s11064-025-04499-4","url":null,"abstract":"<div><p>Perioperative neurocognitive disorders (PND) are linked to neuroinflammation, a key factor in hypertension, but their causal relationship is underexplored. This study aims to investigate whether hypertension is a risk factor for PND, identify related neuroinflammatory targets, and determine if the angiotensin receptor blockers (ARBs) candesartan can improve cognitive function in PND mouse models by modulating these targets. This study identified hypertension as a risk factor for cognitive dysfunction (OR = 1.0767, <i>P</i> = 0.0057) through Mendelian randomization (MR) analysis. Subsequently, bioinformatics techniques were employed to identify the neuroinflammatory targets associated with hypertension for ARBs. Differential analysis revealed Bdkrb1, Ccr1, and Thbs1 were PND biomarkers associated with hypertension, confirmed by machine learning and receiver operating characteristic (ROC) analysis (area under the curve (AUC) &gt; 0.9). Immune infiltration showed Thbs1 positively correlated with MoDC cells (<i>r</i> = 0.70), while Bdkrb1 negatively correlated with Plasma cells (<i>r</i> = -0.75). In the PND mouse model, we assessed whether candesartan could inhibit the onset of neuroinflammation by modulating the targets identified through our screening process. Molecular experiments, including RT-qPCR, Western blotting, immunofluorescence, and ELISA, analyzed gene expression and neuroinflammatory changes in the hippocampus. In a PND mouse model, candesartan improved cognitive function, reducing escape latency and increasing spontaneous alternation rates. Molecular analysis demonstrated candesartan downregulated Bdkrb1 and Ccr1 expression while upregulating Thbs1 in the hippocampus. Additionally, candesartan reduced IL-1β, IL-6, TNF-α levels and microglial activation, highlighting its anti-inflammatory and neuroprotective effects in PND. In conclusion, candesartan improved cognitive function in PND mice by modulating Bdkrb1, Ccr1, and Thbs1, reducing neuroinflammation, and targeting hippocampal immune responses, highlighting its therapeutic potential for PND.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12307533/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726408","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":"Intranasal Terpene Treatment for Glioblastoma: the Neuro-Oncological Potential of Perillyl Alcohol","authors":"Emirhan Harbi,&nbsp;Erhan Yarar,&nbsp;Christopher E. Mason,&nbsp;Michael Aschner,&nbsp;Aytug Altundag","doi":"10.1007/s11064-025-04505-9","DOIUrl":"10.1007/s11064-025-04505-9","url":null,"abstract":"<div><p>Glioblastoma is the most aggressive and fatal primary brain tumor in adults, characterized by poor prognosis and limited treatment efficacy due to the impermeability of the blood-brain barrier (BBB) and its treatment-resistant nature. This review aims to evaluate the potential of intranasal terpene treatment (ITT) as a novel and non-invasive strategy to bypass the BBB and improve glioblastoma treatment outcomes. A review of recent preclinical and clinical studies on intranasally administered compounds (especially terpenes such as Perillyl alcohol (POH)) is presented in terms of their molecular mechanisms, bioavailability, and clinical effects in the central nervous system (CNS).</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726410","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":"Mitochondrial Damage and Autophagy Dysregulation in Alzheimer’s Disease: Mechanisms and Therapeutic Opportunities","authors":"Qian Yu,&nbsp;Li Li,&nbsp;Shuyi Yu,&nbsp;Jialin Han,&nbsp;Qian Cheng,&nbsp;Zhikang Cui,&nbsp;Hang Chen,&nbsp;Ming Li,&nbsp;Zhiming Lu","doi":"10.1007/s11064-025-04490-z","DOIUrl":"10.1007/s11064-025-04490-z","url":null,"abstract":"<div><p>Alzheimer's disease (AD) is a neurodegenerative disorder that causes progressive neurodegeneration and a variety of cognitive deficits. Of note, mitochondrial malfunctions occur early in the disease's development. Mitophagy impairment leads to the build-up of damaged mitochondria inside the cells, causing malfunction and eventual death of the cells. This review summarizes the mechanisms linking mitochondrial damage and autophagy dysregulation to AD and highlights potential therapeutic opportunities. We summarize how mitochondrial dysfunction contributes to AD, including defects in mitochondrial biogenesis, impaired dynamics, the impact of AD-related protein aggregates on mitochondrial integrity, and defective axonal transport. We also explore the roles of mitophagy in AD, including its function in the removal of harmed proteins and organelles. Finally, we highlight the therapeutic strategies for the treatment of AD, targeting molecular components involved in mitochondrial damage and autophagy dysregulation in AD, i.e., antioxidants, mitochondrial modulators, and mitophagy enhancers.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726411","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":"Polycyclitol Derivatives Restore Long- Term Memory Via cdk5/p25 Activation of Tau Signaling in Experimental Cerebral Malaria","authors":"Praveen Kumar Simhadri,&nbsp;Showkat Rashid,&nbsp;Shailaja Karri,&nbsp;Bilal A. Bhat,&nbsp;Goverdhan Mehta,&nbsp;Phanithi Prakash Babu","doi":"10.1007/s11064-025-04495-8","DOIUrl":"10.1007/s11064-025-04495-8","url":null,"abstract":"<div><p>Cyclin-dependent kinase 5 (Cdk5), a purified form of tau protein kinase II (TPKII), mediates abnormal tau hyperphosphorylation through activation by its cofactor p25. The resulting Cdk5-p25 complex promotes the production of the pro-inflammatory cytokine IL-1β, contributing to elevated expression of the microglial marker Iba-1, an established feature of tauopathy-driven neurodegenerative diseases. Hyperphosphorylation of tau at Ser396/404 disrupts microtubule stability, leading to neuronal dysfunction, synaptic loss, and cognitive deficits. Notably, approximately 25% of children surviving cerebral malaria in Sub-Saharan Africa experience cognitive impairments, underscoring the urgent need for neuroprotective therapies. In this study, we employed an experimental cerebral malaria model to assess the therapeutic potential of four polycyclic derivatives, <b>SR4-01</b> to <b>SR4-04</b>, as adjuncts to artemether. We evaluated their efficacy in attenuating Cdk5-p25-mediated tau hyperphosphorylation at Ser396, with the goal of restoring neuronal architecture and cognitive function. Behavioral assessments included the Barnes maze for long-term memory, T-maze for short-term memory, and a novelty-based recognition task. Among the treatment groups, <b>SR4-02</b> and <b>SR4-04</b> demonstrated significant improvements in learning and memory compared to both artemether monotherapy and the <b>SR4-01</b> and <b>SR4-03</b> groups. Immunohistochemical analysis of the hippocampus and cortex showed reduced phospho-tau (Ser396) expression in the <b>SR4-02</b> and <b>SR4-04</b> groups. Golgi-Cox staining further revealed enhanced neuronal arborization in the CA1 and CA3 subregions of the hippocampus and in the cortex. Western blot analysis confirmed reduced Cdk5-p25-mediated tau phosphorylation in the <b>SR4-04</b> treated group. Collectively, our findings suggest that <b>SR4-02</b> and <b>SR4-04</b> hold promise as adjunctive therapies for reducing tau pathology and restoring cognitive function in cerebral malaria-associated neurodegeneration.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144717157","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":"Avocado Oil Prevents Neurological and Behavioral Alterations in a Quinolinic Acid-Induced Model of Huntington’s Disease","authors":"Edith González-Guevara,&nbsp;Pablo Eliasib Martínez-Gopar,&nbsp;Alicia Sánchez-Mendoza,&nbsp;Quetzalli Denisse Angeles-López,&nbsp;Diego López-Orozco,&nbsp;Luis Tristán-López,&nbsp;Mohammed El-Hafidi,&nbsp;Mitzi Daniela Becerril-Cavazos,&nbsp;Claudia Peña-Segura,&nbsp;Carlos Alfredo Silva-Islas,&nbsp;Francisca Pérez-Severiano","doi":"10.1007/s11064-025-04496-7","DOIUrl":"10.1007/s11064-025-04496-7","url":null,"abstract":"<div>\u0000 \u0000 <p>Avocado oil is a nutraceutical that offers multiple health benefits due to its rich composition of fatty acids. Avocado’s antioxidant molecules can protect from neuronal damage, potentially preventing or slowing down the onset of neurodegenerative diseases. Within the search for therapeutic targets in neurodegenerative conditions, we focused on testing the neuroprotective effect of the components contained in avocado oil in a Huntington’s disease (HD) model. Quinolinic acid (QA) is a potent striatal excitotoxin that leads to axon-sparing neurodegeneration and induces N-methyl-D-aspartate receptor-mediated cytotoxicity and neuroinflammation. The QA-lesioned rat striatum shares similarities with the neostriatum observed in individuals with HD. This work aimed to study the neuroprotective effects of an avocado oil-supplemented diet on the QA model by measuring neurological and oxidative damage. For this purpose, Wistar rats were fed with an avocado oil-supplemented diet for 20 days. First, evaluated blood biochemical parameters (glucose, cholesterol, and triglycerides) in the blood and testing liver function by the determination of hepatic enzymes levels in plasma and verifying that the avocado oil-supplemented diet did not affect either. Additionally, a second set of rats were fed with an avocado oil-supplemented diet and then lesioned with QA. Our results show that avocado oil supplementation reduces oxidative damage, prevents neurological damage by reducing the ipsilateral turns by maintaining the levels of striatal GABA content, and reduces striatal neurodegeneration assessed by Fluoro-Jade^® B. These results suggest that an avocado oil-supplemented diet has a potential role in reducing the negative effects observed in the HD model of the QA intrastriatal administration.</p>\u0000 </div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144697248","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":"Correction: The Neuroprotective Impact of Agomelatine in Preserving Brain Tissue Molecular Structure Against Alzheimer’s Disease Etiology","authors":"Sarah S. Amin,&nbsp;Safaa Qusti,&nbsp;Waad A. Al-Otaibi,&nbsp;Sahar M. AlMotwaa,&nbsp;Norah T. S. Albogamy,&nbsp;Madeha N. Alseeni,&nbsp;Eida M. Alshammari,&nbsp;Manal A. Babaker,&nbsp;Abdu Saeed","doi":"10.1007/s11064-025-04501-z","DOIUrl":"10.1007/s11064-025-04501-z","url":null,"abstract":"","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144688556","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}