Metabolic brain disease最新文献_第4页

Mitochondria-targeted antioxidant skq1 reverses functional impairment and histopathological insults in a chronic animal model of multiple sclerosis. 线粒体靶向抗氧化剂skq1在多发性硬化症慢性动物模型中逆转功能损伤和组织病理学损伤。

IF 3.5 3区医学

Metabolic brain disease Pub Date : 2025-08-22 DOI: 10.1007/s11011-025-01676-w

Amin Zolfaghari, Ameneh Omidi, Maliheh Soodi

{"title":"Mitochondria-targeted antioxidant skq1 reverses functional impairment and histopathological insults in a chronic animal model of multiple sclerosis.","authors":"Amin Zolfaghari, Ameneh Omidi, Maliheh Soodi","doi":"10.1007/s11011-025-01676-w","DOIUrl":"https://doi.org/10.1007/s11011-025-01676-w","url":null,"abstract":"Multiple sclerosis (MS) is the most prevalent demyelinating disorder of the central nervous system (CNS), manifested by motor impairments. Due to the critical role of mitochondrial dysfunction, this study investigated the effects of the mitochondria-targeted antioxidant SkQ1 on a mouse model of MS. Animals were categorized into the control group (CONT), the cuprizone group (CPZ), and the group receiving mitochondria-targeted antioxidant SkQ1 following cuprizone (CPZ + SkQ1). After behavioral assessment, the corpus callosum underwent histopathological, biochemical, and molecular evaluations. The behavioral assessment showed a considerable motor improvement in the CPZ + SkQ1 mice compared to the CPZ group. Histopathological investigations revealed significantly higher remyelination in the corpus callosum of CPZ + SkQ1 mice than in the CPZ group. Evaluation of oxidative stress levels showed that SkQ1 administration resulted in a statistical increase in the superoxide dismutase, catalase, and total thiols but a decrease in the malondialdehyde concentration compared to the CPZ group. The relative gene expression level for myelin-related genes significantly increased in the CPZ + SkQ1 group compared to the CPZ group. The findings of this study demonstrate that mitochondria-targeted antioxidant SkQ1 may, through targeting oxidative stress in the mitochondria and consequently myelin gene expression, have induced remyelination enhancement and improved functional performance in chronic cuprizone-intoxicant mice.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 7","pages":"249"},"PeriodicalIF":3.5,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961457","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}

引用次数: 0

Mechanistic study on ligustilide modulation of the TLR4/NF-κB pathway in ameliorating Scopolamine-Induced cognitive impairment. 川芎内酯调节TLR4/NF-κB通路改善东莨菪碱所致认知障碍的机制研究。

IF 3.5 3区医学

Metabolic brain disease Pub Date : 2025-08-15 DOI: 10.1007/s11011-025-01672-0

Qian Zhang, Minghuang Gao, Ziqiao Xu, Jiaqi Xu, Guangcheng Zhong, Hongying Yang, Cong Yang, Qi Wang

{"title":"Mechanistic study on ligustilide modulation of the TLR4/NF-κB pathway in ameliorating Scopolamine-Induced cognitive impairment.","authors":"Qian Zhang, Minghuang Gao, Ziqiao Xu, Jiaqi Xu, Guangcheng Zhong, Hongying Yang, Cong Yang, Qi Wang","doi":"10.1007/s11011-025-01672-0","DOIUrl":"10.1007/s11011-025-01672-0","url":null,"abstract":"This research employed a multi-method strategy integrating network pharmacology, molecular docking, and animal experiments to investigate the therapeutic mechanisms of ligustilide in Alzheimer's disease (AD) management. AD-related targets were obtained from GeneCards, while ligustilide-associated targets were identified using SwissTargetPrediction. Protein interaction networks were constructed via the STRING database. Functional annotation and pathway enrichment analysis were performed using Metascape, including Gene Ontology and KEGG pathway analyses revealing that ligustilide modulated AD progression primarily by regulating the Toll-like receptor 4/nuclear factor kappa B (TLR4/NF-κB) signaling pathway. Molecular docking studies conducted with AutoDock Vina demonstrated strong binding affinities between ligustilide and key targets in this pathway. Behavioral evaluations, including locomotor activity assessment (open field test), spatial memory analysis (Morris water maze), and recognition memory testing (novel object recognition test) demonstrated that ligustilide significantly attenuated SCOP-induced cognitive deficits. Histopathological and biochemical analyses indicated that ligustilide maintained cholinergic neuron integrity and boosted antioxidant defenses in SCOP-treated mice. Transcriptional profiling revealed decreased expression of TLR4, NF-κB p65, and pro-inflammatory mediators (TNF-α, IL-1β, IL-6) in ligustilide-treated AD model mice. Western blot and enzyme-linked immunosorbent assay (ELISA) demonstrated reduced levels of TLR4, phosphorylated p65 (Ser536), TNF-α, IL-1β and IL-6 in ligustilide-treated AD model mice. These findings collectively demonstrate that ligustilide alleviates SCOP-induced cognitive deficits through suppression of the TLR4/NF-κB signaling cascade.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 6","pages":"248"},"PeriodicalIF":3.5,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144855799","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}

引用次数: 0

A tetrahydropyrimidine derivative demonstrates neuroprotection against ketamine-induced schizophrenia through moderating oxidative and inflammatory markers. 四氢嘧啶衍生物通过调节氧化和炎症标志物显示对氯胺酮诱导的精神分裂症的神经保护作用。

IF 3.5 3区医学

Metabolic brain disease Pub Date : 2025-08-14 DOI: 10.1007/s11011-025-01651-5

Tayyaba Tahir, Qurat-Ul-Ain, Ammara Saleem, Shahnaz, Muhammad Imran Khan, Kanwal Akhtar, Irfan Hamid, Rabia Iqbal, Zulcaif Ahmad, Muhammad Furqan Akhtar

{"title":"A tetrahydropyrimidine derivative demonstrates neuroprotection against ketamine-induced schizophrenia through moderating oxidative and inflammatory markers.","authors":"Tayyaba Tahir, Qurat-Ul-Ain, Ammara Saleem, Shahnaz, Muhammad Imran Khan, Kanwal Akhtar, Irfan Hamid, Rabia Iqbal, Zulcaif Ahmad, Muhammad Furqan Akhtar","doi":"10.1007/s11011-025-01651-5","DOIUrl":"10.1007/s11011-025-01651-5","url":null,"abstract":"Schizophrenia impacts individuals' cognition, perceptions, behavior and memory and influences almost 1-1.5% of the global population. It is a psychotic disorder possibly caused by high levels of immunostimulants as well as oxygen-derived free radicals in the blood and CSF. As observed in the studies that pyrimidine derivatives (THP) have promising potential to act as anti-inflammatory agents, therefore these may be helpful in treating schizophrenia. So, this study evaluated the preventive potential of THP in treating schizophrenia induced by ketamine. The mice were segregated in six groups, normal control received 0.5% CMC 1 ml/kg I.P.), disease control and other groups received ketamine 10 mg/kg I.P. Clozapine (1 mg/kg I.P.) served as standard drug. Other groups received THP (10 mg/kg/day I.P.), THP (15 mg/kg/day I.P.) and THP (20 mg/kg/day I.P.). Study was designed as a preventive trial spanning 21-days with initial 14 days treatment, followed by a subsequent 7-day ketamine administration. The study demonstrated that the improvement of positive, negative and cognitive symptoms in THP-treated animals by significantly reducing stereotypic behaviors and inactivity in forced swim and tail suspension tests, and accelerating center time in Open field test and number of entries and alteration in Y-maze test. Oxidative stress in schizophrenic mice was also managed by marked elevation in SOD and CAT levels, and the parameters like GSH, MDA and nitrite contents were significantly reduced. In addition, inflammatory markers such as TNF-α, IL-6, NF-κB and MAP-K were significantly reduced. Furthermore, gene expression showed significant incline in BDNF levels, after THP administration in schizophrenic mice. Overall, the study disclosed THP as an effective compound in mitigating the symptoms of schizophrenia, however further study is needed to evaluate its toxicity profile.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 6","pages":"247"},"PeriodicalIF":3.5,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144855798","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}

引用次数: 0

Neuroprotective effects of resveratrol and sodium valproate in penicillin-induced epilepsy model. 白藜芦醇和丙戊酸钠对青霉素致癫痫模型的神经保护作用。

IF 3.5 3区医学

Metabolic brain disease Pub Date : 2025-08-04 DOI: 10.1007/s11011-025-01667-x

Elif Azize Özşahin Delibaş, Zeynep Kasap Acungil, Fikret Gevrek

{"title":"Neuroprotective effects of resveratrol and sodium valproate in penicillin-induced epilepsy model.","authors":"Elif Azize Özşahin Delibaş, Zeynep Kasap Acungil, Fikret Gevrek","doi":"10.1007/s11011-025-01667-x","DOIUrl":"10.1007/s11011-025-01667-x","url":null,"abstract":"This study investigated resveratrol's (RSV) neuroprotective properties in a penicillin-mediated epilepsy model, focusing on its anti-oxidation, anti-inflammatory, and anti-apoptotic properties, as well as its potential molecular interactions with an anti-epileptic drug sodium valproate (VPA). Thirty-two Wistar albino rats were divided into 4 groups; (PG) Penicillin 500 IU (2.5 µL, i.c.), (RG) RSV 40 mg/kg (i.p.) + Penicillin 500 IU (2.5 µL, i.c.), (SVG) Sodium VPA 300 mg/kg (i.p.) + Penicillin 500 IU (2.5 µL, i.c.), and (RSVG) RSV 40 mg/kg (i.p.) + Sodium VPA 300 mg/kg (i.p.) + Penicillin 500 IU (2.5 µL, i.c.). Anti-oxidation/anti-inflammatory aspects of RSV were evaluated by measuring malondialdehyde (MDA), protein carbonyl compounds (PCC), high mobility group box-1 (HMGB1), and nuclear factor-κappaB (NF-κB) levels using the ELISA method. Apoptosis in epilepsy was determined using the TUNEL method. Plasma MDA levels significantly decreased in RG and RSVG compared to PG, whereas tissue MDA levels significantly decreased in RSVG compared to PG. Plasma HMGB-1 and NF-κB levels significantly decreased in RG and RSVG compared to PG. Penicillin administration caused apoptosis in hippocampal CA1, CA2, CA3, and DG regions, with significant decrease in cell damage in RG and RSVG compared to PG and SVG groups (p < 0.05). This study suggests that RSV co-administered with sodium VPA may reduce oxidative stress/inflammation-induced neuronal death by decreasing MDA, HMGB1, and NF-κB levels, potentially offering a synergistic neuroprotective alternative for epileptogenic brain injury treatment.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 6","pages":"246"},"PeriodicalIF":3.5,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144784780","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}

引用次数: 0

The evaluation of maternal immune activation and the development of schizophrenia in offspring of rats. 母系免疫激活与大鼠后代精神分裂症发展的评价。

IF 3.5 3区医学

Metabolic brain disease Pub Date : 2025-08-02 DOI: 10.1007/s11011-025-01670-2

Lara Canever, Tathiane Alves Lima Evangelista, Octacilio Calixto, Gustavo Antunes Mastella, Amanda Kunz Godoi, Daniele Celso, Samira S Valvassori, Jorge M Aguiar-Geraldo, Taise Possamai-Della, João Pedro Veronezi, Alexandra I Zugno

引用次数: 0

Optimizing predictive biomarkers for alzheimer's disease: muscarinic M1 antagonist-induced synaptic signaling disruptions and bee venom intervention through cholinergic modulation and multiregression dose selection. 优化阿尔茨海默病的预测生物标志物：毒蕈碱M1拮抗剂诱导的突触信号中断和蜂毒通过胆碱能调节和多回归剂量选择进行干预。

IF 3.5 3区医学

Metabolic brain disease Pub Date : 2025-07-29 DOI: 10.1007/s11011-025-01663-1

Hajir A Al Saihati, Naema Ibolgasm Alazabi, Rofanda M Bakeer, Ghada M Abol-Fetouh, Omar A Ahmed-Farid, Alhanouf F Alshedi, Nimer F Alsabeelah

{"title":"Optimizing predictive biomarkers for alzheimer's disease: muscarinic M1 antagonist-induced synaptic signaling disruptions and bee venom intervention through cholinergic modulation and multiregression dose selection.","authors":"Hajir A Al Saihati, Naema Ibolgasm Alazabi, Rofanda M Bakeer, Ghada M Abol-Fetouh, Omar A Ahmed-Farid, Alhanouf F Alshedi, Nimer F Alsabeelah","doi":"10.1007/s11011-025-01663-1","DOIUrl":"10.1007/s11011-025-01663-1","url":null,"abstract":"Alzheimer's (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and neurochemical imbalances. The present study aims to ensure the correct dosage of scopolamine (SC) for inducing AD using Quality by Design to optimize the predictive biomarker acetylcholine esterase. Further, neuroprotective effects will be assessed with variable doses of bee venom (BV) by analyzing its effect on cognitive function, neurochemical markers, and oxidative stress. The goal of this study is to improve models of AD and learn more about how BV can protect neurons in a dose-dependent way during treatment. Methods: The rats were randomly divided into six groups (n = 6): Control, SC -induced AD, SC + Memantine (1 mg/kg bwt p.o.), and three BV doses (5, 10, 15 µl/kg, i.p, every other day) to study dose-dependent effects combined with SC. Memantine and BV were given to the animals two months before they developed AD, which happened on its own 14 days after treatment. After four days of behavioral assessment using the Morris Water Maze to evaluate cognitive function, the animals were humanely sacrificed. Blood and brain samples were collected for the measurement of serum liver and kidney function markers, oxidative and nitrosative stress parameters, cellular energy metabolites, amino acid profiles, neurotransmitters, and inflammatory markers in brain tissue. Results and Conclusion: The most remarkable neuroprotective effect was found in the group treated with BV medium and high dose showed a plateau, beyond which no more improvement was shown. These findings point toward a promising therapeutic approach for BV in the cognitive decline of AD.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 6","pages":"244"},"PeriodicalIF":3.5,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144732348","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}

引用次数: 0

Correction to: Non-invasive remote ischemic postconditioning stimulates neurogenesis during the recovery phase after cerebral ischemia. 纠正：无创远端缺血后处理刺激脑缺血恢复期的神经发生。

IF 3.5 3区医学

Metabolic brain disease Pub Date : 2025-07-29 DOI: 10.1007/s11011-025-01666-y

Dan Huang, Honghong Liu, Yun Qu, Pu Wang

引用次数: 0

Exploration of Imatinib involved in amyloidogenesis as a common foundation for type-2 diabetes mellitus (T2DM) and Alzheimer's disease (AD). 伊马替尼参与淀粉样蛋白形成作为2型糖尿病（T2DM）和阿尔茨海默病（AD）的共同基础的探索

IF 3.5 3区医学

Metabolic brain disease Pub Date : 2025-07-21 DOI: 10.1007/s11011-025-01664-0

Ashi Mannan, Shareen Singh, Maneesh Mohan, Thakur Gurjeet Singh

{"title":"Exploration of Imatinib involved in amyloidogenesis as a common foundation for type-2 diabetes mellitus (T2DM) and Alzheimer's disease (AD).","authors":"Ashi Mannan, Shareen Singh, Maneesh Mohan, Thakur Gurjeet Singh","doi":"10.1007/s11011-025-01664-0","DOIUrl":"10.1007/s11011-025-01664-0","url":null,"abstract":"Diabetes patients have reduced basal cognitive abilities like learning, memory, and perceptual quickness, as well as a 65 percent higher risk of acquiring AD. AD and diabetes share a number of risk factors, including elevated cholesterol, Aβ deposition, degeneration, inflammation, oxidative stress, cardiovascular diseases, dysmetabolism syndrome, τ-protein phosphorylation, glycogen synthesis kinase 3, apoptosis and apolipoprotein E4. This study explores the potential inhibitory effects of imatinib at doses of 1 and 5 mg/kg, with a particular emphasis on the role of c-Abl in amyloidogenesis, a common mechanism that underlies T2DM and AD. Induction of T2DM induced AD by HFD-STZ-Aβ25-35 model. Assessment of behavioural parameters like polydipsia, polyphagia, morris water maze & passive avoidance test; biochemical estimation of glucose, insulin, oxidative stress (SOD, GSH, Cat, TBARS), neuroinflammation (IL-1β, IL-6, TNF-α, NF-κβ), Aβ levels, c-Abl through ELISA technique. Imatinib (1 & 5 mg/kg) results in a reduction in food and water intake, as well as a reduction in memory impairment in the Morris water maze and passive avoidance test. Further, it normalises glucose, insulin, and anti-oxidant elements (SOD, GSH, Cat) levels, while decreasing TBARS levels. Additionally, ELISA data demonstrated a reduction in neuroinflammation (downregulation of IL-1β, IL-6, TNF-α, and NF-κβ), Aβ accumulation, and c-Abl levels by imatinib (1 & 5 mg/kg). Consequently, c-Abl can play a crucial role in the mediation of amyloidogenesis induced by T2DM, thereby establishing a connection between T2DM and AD. Therefore, Imatinib has the potential to treat and prevent the progression of T2DM to AD.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 6","pages":"242"},"PeriodicalIF":3.5,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675287","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}

引用次数: 0

Paeoniflorin and depression: a comprehensive review of underlying molecular mechanisms. 芍药苷与抑郁症：潜在分子机制的综合综述。

IF 3.5 3区医学

Metabolic brain disease Pub Date : 2025-07-19 DOI: 10.1007/s11011-025-01671-1

Priya Sahani, Lovedeep Singh

{"title":"Paeoniflorin and depression: a comprehensive review of underlying molecular mechanisms.","authors":"Priya Sahani, Lovedeep Singh","doi":"10.1007/s11011-025-01671-1","DOIUrl":"10.1007/s11011-025-01671-1","url":null,"abstract":"Depression is one of the common mental disorders that often leads to persistent low mood, feelings of sadness or a sense of hopelessness, disinterest, or lack of pleasure in most day-to-day things. Depression is a leading cause of disability worldwide and a major contributor to the global burden of disease. Depression is a multifactorial disorder involving several interlinked pathways. A decrease in BDNF impairs neuroplasticity and synaptic function. Overactivation of the HPA axis elevates cortisol and disrupts mood regulation. Whereas/TLR-4/NF-κB activation triggers neuroinflammation, while NLRP3 inflammasome activation induces pyroptosis, promoting neuronal damage. Besides this, oxidative stress from ROS/antioxidant imbalance leads to neuronal damage and exacerbates neuroinflammatory responses. Moreover, reduced biogenic amines (like serotonin and dopamine) weaken mood regulation, and increased glutamatergic transmission leads to excitotoxicity. Together, these alterations contribute to the onset and progression of depression, necessitating a multifaceted approach. Paeoniflorin is a monoterpene glycoside isolated from the aqueous extract of the dry root of Paeonia species such as Paeonia lactiflora, Paeonia suffruticosa, and Paeonia veitchii. It exhibits a wide range of pharmacological activities, including antidepressant. anti-inflammatory, antioxidant, anticonvulsive, analgesic and hepatoprotective activities. Various reports have delineated that paeoniflorin exerts antidepressant effects by modulating the crucial mediators implicated in the pathophysiology of depression, including BDNF, CREB, NF-κB, TLR-4, NLRP3, HPA axis, ROS, serotonin, glutamate, mTOR, HMGB1, caspases, and SNARE proteins, among others, thereby providing a multitargeted defense against depression. Considering the potential of paeoniflorin in modulating these mediators, the current review is structured to explore the mechanistic interplay among these pathways in mediating its antidepressant effects.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 6","pages":"241"},"PeriodicalIF":3.5,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667997","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}

引用次数: 0

From nonalcoholic fatty liver disease to neuroinflammation: the role of chronic systemic inflammation. 从非酒精性脂肪肝到神经炎症：慢性全身性炎症的作用

IF 3.5 3区医学

Metabolic brain disease Pub Date : 2025-07-10 DOI: 10.1007/s11011-025-01669-9

Xupeng Huang, Ziqi Sang, Haifeng Liu, Jia Yang, Kuisong Wang, Yanan Qu, Houbo Deng

{"title":"From nonalcoholic fatty liver disease to neuroinflammation: the role of chronic systemic inflammation.","authors":"Xupeng Huang, Ziqi Sang, Haifeng Liu, Jia Yang, Kuisong Wang, Yanan Qu, Houbo Deng","doi":"10.1007/s11011-025-01669-9","DOIUrl":"10.1007/s11011-025-01669-9","url":null,"abstract":"Neuroinflammation is a significant contributor to neurological disorders. While previous research has mainly concentrated on lesions within the brain, the potential influence of nonalcoholic fatty liver disease (NAFLD) on neuroinflammation has been largely overlooked. An increasing amount of evidence suggests that heightened chronic systemic inflammation linked to NAFLD could significantly contribute to the initiation and advancement of neuroinflammation, nonetheless, the underlying mechanisms remain unclear. This review summarizes the primary causes of chronic systemic inflammation in the context of NAFLD, delineates the mechanisms by which chronic systemic inflammation leads to neuroinflammation, analyzes the key pathways through which circulating inflammatory mediators travel from the periphery to the central nervous system and their effects on glial cells, and finally discusses the novel approaches for treating neuroinflammation via a liver-brain inflammation axis perspective. This research intends to offer an in-depth insight into how chronic systemic inflammation contributes to the connection between NAFLD and neuroinflammation.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 6","pages":"240"},"PeriodicalIF":3.5,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12245968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144600971","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}

引用次数: 0