Metabolic brain disease最新文献

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 3.2 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":"https://doi.org/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":3.2,"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 3.2 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":"https://doi.org/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":3.2,"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 3.2 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":3.2,"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

Neuroprotective effects of Simvastatin against alcohol-induced oxidative stress and neurodegeneration in the Hippocampus of adolescent mice. 辛伐他汀对酒精诱导的氧化应激和青春期小鼠海马神经变性的神经保护作用。

IF 3.2 3区医学

Metabolic brain disease Pub Date : 2025-07-09 DOI: 10.1007/s11011-025-01668-w

Robin du Preez, Tabo Mwila, Alice Efuntayo, Oladiran I Olateju

{"title":"Neuroprotective effects of Simvastatin against alcohol-induced oxidative stress and neurodegeneration in the Hippocampus of adolescent mice.","authors":"Robin du Preez, Tabo Mwila, Alice Efuntayo, Oladiran I Olateju","doi":"10.1007/s11011-025-01668-w","DOIUrl":"10.1007/s11011-025-01668-w","url":null,"abstract":"Adolescent alcohol abuse in disadvantaged communities is a significant concern due to regulatory gaps. It disrupts brain development, particularly affecting the hippocampus, which is vulnerable to alcohol-induced oxidative stress, resulting in impaired neuronal signalling, increased cell death, and reduced neurogenesis. Simvastatin, a cholesterol-lowering drug, has neuroprotective and antioxidant effects, but its potential in protecting against alcohol-related brain damage is unclear. This study examined the protective effects of Simvastatin in four-week-old C57BL/6J mice administered 20% alcohol (intraperitoneal, i.p.), 5 or 15 mg/kg Simvastatin orally, followed by 20% alcohol (i.p.) or the controls (i.e., 5 mg/kg Simvastatin only or no treatment). After 28 days, the harvested brains underwent biochemical or immunohistochemical (IHC) analysis. Biochemical analyses measured malondialdehyde (MDA) levels, glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activity in homogenised hippocampal samples and IHC involved immunolabelling for PcNA or DCX. PcNA- or DCX-positive cells in the suprapyramidal blade of the dentate gyrus were counted using QuPath software. Alcohol elevated GSH-Px activity, indicating oxidative damage, but both Simvastatin concentrations reduced this, with 15 mg being more effective in females. MDA level and SOD activity remained unchanged. Simvastatin at 5 mg reduced alcohol's effect on PcNA-positive cells in both sexes, while 15 mg was more effective in females. For DCX-positive cells, 5 mg Simvastatin was protective in both sexes, but 15 mg showed no effect. Overall, Simvastatin exhibited antioxidant and neuroprotective effects against alcohol-induced hippocampal damage, suggesting its potential for treating alcohol-related brain disorders.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 6","pages":"239"},"PeriodicalIF":3.2,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12241278/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144591703","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

Mechanistic study of butylphthalide in alleviating cerebral Edema after intracerebral Hemorrhage by regulating miR-7-5p expression. 丁苯酞通过调节miR-7-5p表达减轻脑出血后脑水肿的机制研究。

IF 3.2 3区医学

Metabolic brain disease Pub Date : 2025-07-01 DOI: 10.1007/s11011-025-01659-x

Xiqian Chen, Shige Wang, Qiang Lei, Jia Liu, Wei Lu

{"title":"Mechanistic study of butylphthalide in alleviating cerebral Edema after intracerebral Hemorrhage by regulating miR-7-5p expression.","authors":"Xiqian Chen, Shige Wang, Qiang Lei, Jia Liu, Wei Lu","doi":"10.1007/s11011-025-01659-x","DOIUrl":"https://doi.org/10.1007/s11011-025-01659-x","url":null,"abstract":"Objective: To investigate the mechanisms by which butylphthalide (NBP) alleviates cerebral edema after intracerebral hemorrhage (ICH) through the regulation of miR-7-5p expression.Methods: An ICH model was generated in CTX-TNA2 rat astrocyte cell lines using hemin intervention. An in vivo ICH model was created by injecting type IV collagenase into the basal ganglia of Sprague-Dawley (SD) rats. The cell/rat models were treated with NBP and/or stattic. The expression of STAT3, miR-7-5p, EGFR, PI3K, AKT, p-AKT, AKT2, AKT3, and AQP4 were assessed using qRT-PCR, Western blotting, and immunofluorescence. Brain water content was measured using the wet-to-dry weight method, and neurological deficits were evaluated using the NSS (neurological severity score).Results: In both the CTX-TNA2 ICH model and the rat ICH model, miR-7-5p expression was significantly reduced, while STAT3, EGFR, AKT, p-AKT, AKT2, AKT3, and AQP4 expression were elevated compared to the blank/sham-operated group. NBP increased the expression of STAT3 and miR-7-5p, while reducing the expression of EGFR, AKT, p-AKT, AKT2, AKT3, and AQP4. NBP also decreased brain water content and improved NSS scores. STAT3 inhibition significantly reduced STAT3 and miR-7-5p expression, increased the expression of EGFR, PI3K, AKT, p-AKT, AKT2, AKT3, and AQP4, and elevated brain water content. NBP can reverse the downregulation of STAT3 and miR-7-5p expression, the upregulation of EGFR/PI3K/AKT axis and AQP4 expression, and the increase in brain water content induced by STAT3 inhibition.Conclusion: NBP alleviates cerebral edema after ICH by upregulating STAT3 expression, thereby increasing miR-7-5p levels and inhibiting the EGFR/PI3K/AKT axis and AQP4 expression.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 6","pages":"238"},"PeriodicalIF":3.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540867","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 efficacy of Talinum triangulare in Cadmium-induced neurotoxicity: involvement of antioxidant defense, anti-inflammatory, dopaminergic, and cholinergic systems. 三角Talinum对镉诱导的神经毒性的神经保护作用：涉及抗氧化防御、抗炎、多巴胺和胆碱能系统。

IF 3.2 3区医学

Metabolic brain disease Pub Date : 2025-06-30 DOI: 10.1007/s11011-025-01655-1

Johnson O Oladele, Ebenezer I O Ajayi, Isaac O Babatunde, Olaide O Awosanya, Oluwaseun T Oladele, Oluwafemi S Atolagbe, Omowumi O Adewale, Oyedotun M Oyeleke

{"title":"Neuroprotective efficacy of Talinum triangulare in Cadmium-induced neurotoxicity: involvement of antioxidant defense, anti-inflammatory, dopaminergic, and cholinergic systems.","authors":"Johnson O Oladele, Ebenezer I O Ajayi, Isaac O Babatunde, Olaide O Awosanya, Oluwaseun T Oladele, Oluwafemi S Atolagbe, Omowumi O Adewale, Oyedotun M Oyeleke","doi":"10.1007/s11011-025-01655-1","DOIUrl":"https://doi.org/10.1007/s11011-025-01655-1","url":null,"abstract":"The incidence of neurotoxicity has been rising recently due to increase exposure to toxic compounds such as Cadmium (Cd). Aqueous leaf extract of Talinum triangulare (AETT) is used in traditional medicine in the treatment of various kinds of diseases. This study sought to examine neuroprotective potential of AETT on cadmium-induced neurotoxicity in rats. Neurotoxicity was induced in rats via oral administration of 5 mg/kg body weight CdCl2 and treated with either 200 mg/kg of AETT or vitamin E for 14 consecutive days. Results revealed that Cd induced behavioural incompetence with marked decrease in motor skills, muscle strength, exploratory activities, and anxiogenic-like phenotype which are vital psychomotor coordination tools. Cd intoxication caused a marked increase in neuronal expression of inflammatory biomarkers (TNF-α, MPO and NO), hydrogen peroxide generation, and lipid peroxidation; with associated decrease in both enzymatic antioxidants (GST, SOD, CAT) and non-enzymatic antioxidants (reduced glutathione). Similarly, decreased in dopamine with concomitant increased in the activity of acetylcholinesterase were observed in Cd-induced rats. Nevertheless, AETT or vitamin E markedly restored behavioural competence, mitigated neuroinflammation, lipid peroxidation and oxidative stress. AETT modulated cholinergic and dopaminergic pathways which improved bioavailability of acetylcholine and dopamine in the brain. Furthermore, AETT displayed better protective effects than vitamin E, this could be because of antioxidant phytochemicals in AETT as showed in the GCMS result. Overall, this study suggested AETT as a potential therapeutic agent in the treatment of neurotoxicity mediated by toxic metals.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 6","pages":"237"},"PeriodicalIF":3.2,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528907","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

Mechanisms of SIRT1/SIRT3-mediated reduction of mitochondrial regeneration and inflammatory response in diabetic cerebral ischemia-reperfusion injury. SIRT1/ sirt3介导的糖尿病脑缺血再灌注损伤中线粒体再生和炎症反应减少的机制

IF 3.2 3区医学

Metabolic brain disease Pub Date : 2025-06-28 DOI: 10.1007/s11011-025-01662-2

Cheng Xin, Ouya Liu, Miao Sun, Ping Han, Xiaowen Li, Qingfeng Niu, Nenghong Ma, Xiao Yang, Changchun Hei, Ping Liu

引用次数: 0