Molecular Neurobiology最新文献

{"title":"Deciphering the Neuroprotective Action of Bee Venom Peptide Melittin: Insights into Mechanistic Interplay.","authors":"Pankaj Kadyan, Lovedeep Singh","doi":"10.1007/s12035-025-04808-6","DOIUrl":"10.1007/s12035-025-04808-6","url":null,"abstract":"<p><p>Neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis, are characterized by progressive loss of neuronal structure and function. These conditions often lead to cognitive decline, motor dysfunction, and ultimately severe impairment of daily activities. A key feature of neurodegenerative diseases is chronic inflammation, which contributes to neuronal damage and exacerbates disease progression. Traditional treatments mainly focus on symptomatic relief rather than addressing the underlying causes, highlighting the need for novel therapeutic approaches. Melittin, a bioactive peptide derived from bee venom, has garnered attention for its multifaceted neuroprotective properties, particularly in the context of neuroinflammatory and neurodegenerative disorders. This review delves into the molecular mechanisms through which melittin exerts neuroprotective effects, with a focus on its ability to modulate neuroinflammation, apoptosis, and neurogenesis. Research indicates that melittin can downregulate pro-apoptotic pathways by inhibiting calpain-mediated activation of apoptosis-inducing factor and Bax, thereby reducing neuronal cell death. Additionally, melittin exerts its neuroprotective effects through the inhibition of neuroinflammatory processes, specifically by downregulating key inflammatory pathways such as NF-κB and MAPK. This modulation leads to decreased production of proinflammatory cytokines and prostaglandins, which are implicated in the pathogenesis of neurodegenerative disorders. Beyond its anti-inflammatory actions, melittin promotes neurogenesis, potentially through the modulation of the BDNF/Trk-B/CREB signaling pathway, which plays a crucial role in neuronal survival and plasticity. These properties suggest that melittin not only provides symptomatic relief but could also address the root causes of neuronal degeneration, presenting a promising avenue for the development of new treatments for neurodegenerative diseases. Further research is required to validate its efficacy and safety in clinical settings.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"8738-8751"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143557299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuropsychiatric Abnormalities in Metabolic Disturbances: Interplay of Adipokines and Neurotransmission.","authors":"So Yeong Cheon, Juhyun Song","doi":"10.1007/s12035-025-04797-6","DOIUrl":"10.1007/s12035-025-04797-6","url":null,"abstract":"<p><p>Metabolic syndrome, with a high global incidence, is characterized by central obesity, elevated fasting blood glucose, high blood pressure, and abnormal lipid levels, including reduced high-density lipoprotein cholesterol and elevated triglycerides. These metabolic dysfunctions can lead to neurotransmitter alterations and dysregulation of the hypothalamic-pituitary-adrenal axis. These changes, in turn, contribute to mental disorders such as depression and anxiety. Adipokines, secreted from adipose tissue, modulate various metabolic processes, neurotransmission, and immune responses. The interplay between adipokines and neurotransmitters may be a critical component underlying the interaction between metabolic abnormalities and mental disorders. This review aims to discuss the brain-metabolism axis, focusing on altered levels of adipokines and neurotransmitters in metabolic and mental disorders.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"8824-8842"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143557305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Conditioned Medium of BMSCs Alleviates H₂O₂-Induced Oxidative Damage in PC12 Cells Through the LDLR Pathway.","authors":"MingDong Li, Zhongquan Fu, Xing Gao, Yuchen Zhang, Zengxin Gao","doi":"10.1007/s12035-025-04804-w","DOIUrl":"10.1007/s12035-025-04804-w","url":null,"abstract":"<p><p>Oxidative damage is pivotal in the pathogenesis and progression of a myriad of neurological disorders. The current study was designed to elucidate the therapeutic potential of conditioned medium from bone marrow-derived mesenchymal stromal cells (BMSC-CM) and to delineate the underlying mechanisms, using a neuronal oxidative injury model for this purpose. Rat pheochromocytoma PC12 cells were exposed to H₂O₂ to establish an oxidative injury model, followed by treatment with BMSC-CM or co-cultivation with BMSCs in a transwell apparatus. The oxidative stress levels pre- and post-intervention or co-cultivation were quantitatively assessed by PCR and western blot analyses. Furthermore, transcriptomic and bioinformatic analyses were used to identify pivotal genes and signaling pathways implicated in the observed effects. Both BMSC-CM treatment and BMSC co-culture decreased oxidative damage and inhibited apoptosis in PC12 cells. Transcriptomic data and enrichment analysis revealed 106 differentially expressed genes between BMSC-CM untreated and treated H₂O₂-exposed PC12 cells, including 67 downregulated and 39 upregulated genes. Notably, the significantly differentially expressed genes were predominantly those involved in lipid metabolism pathways, and the low-density lipoprotein receptor (LDLR) emerged as one statistically significant upregulated gene. The proprotein convertase subtilisin/kexin type 9, a specific inhibitor of LDLR, attenuated the positive effects of BMSC-CM treatment, corroborating that LDLR activation plays a crucial role in mitigating neuronal oxidative damage. The results of this investigation underscore the neuroprotective capacity of BMSC-CM, which we show is mediated through its ability to module lipid metabolism in neuronal cells via the LDLR. Further research into the neuroprotective properties of BMSC-CM could lead to the development of promising therapeutic avenues for neurological diseases characterized by oxidative stress.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"8857-8867"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143567631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurotoxic Effects of Atrazine on Dopaminergic System via miRNAs and Energy-Sensing Pathways.","authors":"Xiaojuan Chen, Xiaomeng Hu, Hongzhan Liu, Jinyi He, Yanshu Li, Xiaofeng Zhang","doi":"10.1007/s12035-025-04822-8","DOIUrl":"10.1007/s12035-025-04822-8","url":null,"abstract":"<p><p>Atrazine (ATR, 2-chloro-4-ethylamino-6-isopropylamino-1,3,5-triazine) is a globally prevalent herbicide known to induce dopaminergic neurotoxicity at high concentrations. MicroRNAs (miRNAs), pivotal in regulating gene expression post-transcriptionally, play essential roles in neuronal differentiation, proliferation, and apoptosis. This study investigates the effects of ATR on the dopaminergic system and behavioral responses in rats, with a particular focus on critical dopaminergic proteins such as tyrosine hydroxylase (TH), nuclear receptor related-1 protein (NURR1), and α-synuclein. The results reveal that ATR exposure significantly reduces the expression of TH and NURR1, while elevating levels of α-synuclein. Through miRNA sequencing and proteomic analysis, we identify alterations in miRNA and protein profiles that are intricately linked to the development of the dopaminergic system. Notably, treatment with ATR results in a marked increase in AMPK levels concurrent with a decrease in miR-322-5p. The differentially expressed genes associated with ATR exposure primarily influence the dopaminergic system by engaging in critical pathways such as AMPK, mTOR, autophagy, FoxO, and HIPPO. This study underscores the neurotoxic impact of ATR on the dopaminergic system via miRNA regulatory mechanisms and energy-sensing pathways, including AMPK and SIRT1, providing a molecular foundation for developing strategies to prevent and treat neurotoxicity induced by ATR exposure.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"9018-9030"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143630547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systematic Identification of Mitochondrial Signatures in Alzheimer's Disease and Inflammatory Bowel Disease.","authors":"Fei Wang, Jiaqi Wang, Tong Chen, Shuaibin Wang, XiangYu Meng, Yin Shen, Xuan Xu","doi":"10.1007/s12035-025-04826-4","DOIUrl":"10.1007/s12035-025-04826-4","url":null,"abstract":"<p><p>Mitochondrial dysfunction is increasingly recognized as a shared feature of Alzheimer's disease (AD) and inflammatory bowel disease (IBD), linked through overlapping pathways of hypoxia and immune dysregulation. Our study integrated transcriptomic and genetic analyses to uncover mitochondria-related mechanisms underlying these diseases. By analyzing multiple AD and IBD datasets through differential expression gene (DEG) analyses, biological pathway enrichment, and co-expression module construction, we identified hypoxia-induced mitochondrial dysfunction as a central risk factor for both conditions. Key findings revealed several mitochondrial-related genes shared between AD and IBD, including BCL6, PFKFB3, NDUFS3, and COX5B, which serve as critical regulators bridging mitochondrial and immune pathways. Drug enrichment analyses using Drug Signatures Database (DsigDB) and the Connectivity Map (cMAP) identified promising therapeutic candidates, including decitabine, DMOG, and estradiol, targeting shared regulators such as BCL6, PFKFB3, MAFF, and TGFBI. These drugs demonstrated potential to modulate mitochondrial autophagy and oxidative phosphorylation (OXPHOS), pathways enriched in the constructed interaction network with BCL6 and PFKFB3 as central nodes. Mendelian randomization (MR) analysis further identified MAP1LC3A as significantly associated with increased risk for both AD and IBD, while NME1 emerged as strongly protective, suggesting their roles as therapeutic targets. Our findings underscore hypoxia-induced mitochondrial dysfunction as a unifying mechanism in AD and IBD, mediated by hypoxia-inducible factor-1α (HIF-1α). By identifying key mitochondria-associated genes and pathways, this study highlights innovative therapeutic targets and contributes to a deeper understanding of the gut-brain interplay in neurodegeneration and chronic inflammation. These insights pave the way for precision medicine strategies targeting mitochondrial dysfunction in AD and IBD.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"9089-9119"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143630517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EIF4A3-Induced circ_0029941 Promotes Astrocyte Activation Through Enhancing Autophagy via miR-224-5p/NFAT5 Axis.","authors":"Chonghua Jiang, Hui Liu, Jun Peng, Xiqi Hu, Ying Xia","doi":"10.1007/s12035-025-04817-5","DOIUrl":"10.1007/s12035-025-04817-5","url":null,"abstract":"<p><p>The abnormal expression of circular RNA (circRNA) has been implicated in the development of many human diseases, including acute ischemic stroke (AIS). However, the role and mechanism of circ_0029941 in AIS progression remain unclear. Transient middle cerebral artery occlusion (tMCAO) was constructed to mimic AIS mice model, and oxygen-glucose deprivation/reoxygenation (OGD/R)-induced astrocytes were used to mimic AIS cell model. The expression of circ_0029941, eukaryotic translation initiation factor 4A-III (EIF4A3), microRNA (miR)-224-5p and nuclear factor activated T cell 5 (NFAT5) were determined by quantitative real-time PCR. Triphenyl tetrazolium chloride staining was used to evaluate infarct size in mice, and immunostaining was performed to confirm GFAP, MAP1LC3B, and NFAT5 levels. Protein expression was tested by western blot analysis, and FISH was used for co-location. The interaction between circ_0029941 and miR-224-5p was verified by RIP and RNA pull-down assays. And the interaction between miR-224-5p and NFAT5 was confirmed by RIP and dual-luciferase reporter assays. Circ_0029941 had elevated expression in AIS patients, tMCAO models and OGD/R-induced astrocytes. Knockdown of circ_0029941 alleviated brain infarction in tMCAO mice. Also, circ_0029941 knockdown inhibited astrocyte activation and ATG5-mediated autophagy. In addition, EIF4A3 promoted circ_0029941 level, and circ_0029941 sponged miR-224-5p to regulate NFAT5. Besides, miR-224-5p inhibitor or NFAT5 overexpression reversed the inhibition effect of circ_0029941 knockdown on astrocyte activation and autophagy. In addition, antagomiR-224-5p also abolished the relieving effect of circ_0029941 knockdown on brain infarction of tMCAO mice. EIF4A3-induced circ_0029941 promoted astrocyte activation and autophagy through regulating the miR-224-5p/NFAT5 axis.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"9175-9189"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143649616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex-Specific Effects of Early-Life Stress Exposure on Memory Performance and the Medial Prefrontal Cortex Transcriptomic Pattern in Adolescent Mice.","authors":"Rodrigo Orso, Thiago Wendt Viola, Bernardo Aguzzoli Heberle, Kerstin Camile Creutzberg, Francisco Sindermann Lumertz, Rodrigo Grassi-Oliveira","doi":"10.1007/s12035-025-04803-x","DOIUrl":"10.1007/s12035-025-04803-x","url":null,"abstract":"<p><p>Early life stress (ELS) is considered a risk factor for the development of cognitive and executive dysfunctions throughout development. The medial portion of the prefrontal cortex (mPFC) is directly implicated in short-term working memory. Furthermore, due to its late development compared to other brain regions, the mPFC is considered a vulnerable brain region to ELS exposure. Here, we investigated the effects of the ELS on PFC-dependent memory and mPFC transcriptomic profiles. From postnatal day (PND) 2 to PND 15, BALB/cJ mice were exposed to maternal separation (MS) for 3 h per day combined with limited bedding (ELS group) or left undisturbed (CT group). During the period of stress, maternal behavior was recorded pre-MS and post-MS. From PND 45 to PND 47, males and females were tested for working memory performance in the Y-maze and short-term recognition memory in the object in place task (OIP). Later, we assessed mRNA level alterations in the mPFC by RNA-seq. Here, we showed that ELS increases maternal care post-MS and the number of nest exits pre-MS and post-MS. Furthermore, males and females exposed to ELS exhibited impairments in the OIP, while only females performed worse in the Y-maze. With respect to the mPFC transcriptome, we identified 13 DEGs in the females, which were significantly influenced by chaperone-mediated protein folding processes, while 4 genes were altered in males. In conclusion, we showed that, compared with male sex, ELS alters maternal behavior and leads to more extensive impairments in memory function and transcriptomic alterations in females.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"8728-8737"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12209009/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143557307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NURR1 Deficiency Is Associated to Altered Microglial Phenotype in Male Mice.","authors":"Francesca Montarolo, Sarah Thielens, Maria Bove, Antonio Bertolotto, Filippo Tempia, Eriola Hoxha","doi":"10.1007/s12035-025-04787-8","DOIUrl":"10.1007/s12035-025-04787-8","url":null,"abstract":"<p><p>The transcription factor NUclear Receptor Related 1 (NURR1) regulates the development and maintenance of midbrain dopaminergic (mDA) neurons, which control voluntary movement, motivation, and reward. NURR1 also plays anti-inflammatory functions in microglia, protecting mDA neurons from inflammation-induced death. It remains to be determined to what extent NURR1 exerts its function in microglia. Interestingly, altered microglial phenotypes are associated to psychiatric conditions. NURR1 defects in male mice are associated with hyperactive and impulsive behaviour. Notably, such behaviour is accompanied by a normal development of mDA neurons which, at least in their number, are preserved. This study aims to explain the altered behaviour of NURR1-deficient mice by analyzing microglial compartment and inflammatory machinery that could be consistently altered to influence such observed behaviours. The present work demonstrates that NURR1 deficiency determines a reduction in the number of microglial cells specifically in the substantia nigra (SN), without altering their morphological activation state. Gene expression levels of molecules associated with active/protective microglial phenotype in the SN of NURR1^+/- mice are altered. The level of HMOX, a marker of cellular damage/apoptosis, is up-regulated, while the level of MT2, a marker of response to stress, is reduced in the SN of NURR1^+/- mice. The level of prostaglandin receptors, which are endogenous ligands for NURR1, is up-regulated in the same compartment. Overall, the NURR1-deficient mice, which exhibit impaired behaviour, have a reduced number of microglia cells and alterations of the inflammatory machinery in their SN.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"8887-8899"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12208995/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ketamine Alters Specific Gene Expression Profiles by Transcriptome-Wide Responses in a Ketamine-Induced Schizophrenia-Like Mouse Model.","authors":"Zhe Du, Xiu-Mei Zhu, Peng Lv, Ying Pan, Xi-Kai Hou, Ang Li, Dong Zhao, Jia-Xin Xing, Jun Yao","doi":"10.1007/s12035-025-04789-6","DOIUrl":"10.1007/s12035-025-04789-6","url":null,"abstract":"<p><p>Psychotic disorder is a significant consequence of ketamine abuse. However, the molecular mechanisms and biomarkers for this psychotic disorder and associated long-term cognitive impairment remain unclear. To investigate the behavioral changes and comprehensive gene expression alterations in mice following ketamine administration, we employed behavioral testing and RNA sequencing (RNA-seq). We further examined the role of dopamine D1 receptor (Drd1) activity in mediating ketamine-induced psychotic-like behavior and its impact on the transcriptome in these mice. Our findings indicated that blocking Drd1 activity with an antagonist mitigated ketamine-induced schizophrenia-like behaviors, while activating Drd1 with an agonist partially replicated these symptoms. Transcriptome analysis of the mouse hippocampus using RNA-seq revealed an enrichment of differentially expressed genes implicated in the GTPase activation pathway. Specifically, both Rgs4 and Gnai3 were involved in ketamine-induced psychiatric effects. Furthermore, we observed that the mRNA expression of Gnai3 was decreased in peripheral blood and the serum levels of eotaxin-2 were elevated two weeks after ketamine administration. These changes suggest that Gnai3 and eotaxin-2 may serve as potential biomarkers for ketamine abuse. These results demonstrate the crucial role of Drd1 activity in a mouse model of ketamine-induced schizophrenia-like disorder. The altered expression of Gnai3 in peripheral blood and the elevated levels of cytokine eotaxin-2 in serum indicate their potential as peripheral blood biomarkers for ketamine abuse in mice.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"8313-8327"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143483595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Benfotiamine Ameliorates Streptozotocin-Induced Alzheimer's Disease in Rats by Modulating Neuroinflammation, Oxidative Stress, and Microglia.","authors":"Camila A E F Cardinali, Yandara A Martins, Ruan C M Moraes, Andressa P Costa, Andréa S Torrão","doi":"10.1007/s12035-025-04811-x","DOIUrl":"10.1007/s12035-025-04811-x","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is the most prevalent cause of dementia, characterized by progressive memory loss and cognitive decline. Recent evidence indicates that inflammation plays a central role in AD pathogenesis, with elevated inflammatory markers and risk genes linked to innate immune functions. Glial cell dysfunction, particularly in astrocytes and microglia, is crucial to the neuroinflammatory process, contributing to oxidative stress, synaptic dysfunction, neuronal death, and impaired neurogenesis. This study aimed to investigate the therapeutic effects of benfotiamine (BFT), a vitamin B1 analogue, on microglial morphology, inflammation, and oxidative stress parameters in a sporadic Alzheimer-like disease model induced by intracerebroventricular injection of streptozotocin (STZ). Supplementation with 150 mg/kg of BFT for 7 days significantly reduced inflammation in the hippocampus and provided protection against oxidative damage in the entorhinal cortex by activating the Nrf-2 pathway and enhancing the expression of antioxidant enzymes such as SOD1 and CAT. These findings suggest that BFT exerts neuroprotective effects in AD, particularly impacting glial cell function and redox homeostasis.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"8695-8717"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143557297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}