Molecular Neurobiology最新文献_第7页

Microglial NLRP3 Inflammasomes in Alzheimer's Disease Pathogenesis: From Interaction with Autophagy/Mitophagy to Therapeutics. 小胶质NLRP3炎性小体在阿尔茨海默病发病机制中的作用：从自噬/自噬相互作用到治疗方法。

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2025-06-01 Epub Date: 2025-02-14 DOI: 10.1007/s12035-025-04758-z

Gunel Ayyubova, Leelavathi N Madhu

{"title":"Microglial NLRP3 Inflammasomes in Alzheimer's Disease Pathogenesis: From Interaction with Autophagy/Mitophagy to Therapeutics.","authors":"Gunel Ayyubova, Leelavathi N Madhu","doi":"10.1007/s12035-025-04758-z","DOIUrl":"10.1007/s12035-025-04758-z","url":null,"abstract":"The nucleotide-binding oligomerization domain-like receptor pyrin domain-containing 3 (NLRP3) inflammasome, discovered 20 years ago, is crucial in controlling innate immune reactions in Alzheimer's disease (AD). By initiating the release of inflammatory molecules (including caspases, IL-1β, and IL-18), the excessively activated inflammasome complex in microglia leads to chronic inflammation and neuronal death, resulting in the progression of cognitive deficiencies. Even though the involvement of NLRP3 has been implicated in neuroinflammation and widely explored in several studies, there are plenty of controversies regarding its precise roles and activation mechanisms in AD. Another prominent feature of AD is impairment in microglial autophagy, which can be either the cause or the consequence of NLRP3 activation and contributes to the aggregation of misfolded proteins and aberrant chronic inflammatory state seen in the disease course. Studies also demonstrate that intracellular buildup of dysfunctional and damaged mitochondria due to defective mitophagy enhances inflammasome activation, further suggesting that restoration of impaired autophagy and mitophagy can effectively suppress it, thereby reducing inflammation and protecting microglia and neurons. This review is primarily focused on the role of NLRP3 inflammasome in the etiopathology of AD, its interactions with microglial autophagy/mitophagy, and the latest developments in NLRP3 inflammasome-targeted therapeutic interventions being implicated for AD treatment.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"7124-7143"},"PeriodicalIF":4.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143414300","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}

引用次数: 0

Potential Ameliorating Effects of Fluvoxamine in a Rat Model of Endotoxin-Induced Neuroinflammation: Molecular Aspects Through SIRT-1/GPX-4 and HMGB-1 Signaling. 氟伏沙明在内毒素诱导的大鼠神经炎症模型中的潜在改善作用：通过SIRT-1/GPX-4和HMGB-1信号传导的分子方面

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2025-06-01 Epub Date: 2025-02-15 DOI: 10.1007/s12035-025-04764-1

Muhammet Yusuf Tepebaşı, Halil Aşcı, Pınar Aslan Koşar, Emine Nur Dinçer, Esma Selçuk, Öznur Kolay, İbrahim Hüseynov

{"title":"Potential Ameliorating Effects of Fluvoxamine in a Rat Model of Endotoxin-Induced Neuroinflammation: Molecular Aspects Through SIRT-1/GPX-4 and HMGB-1 Signaling.","authors":"Muhammet Yusuf Tepebaşı, Halil Aşcı, Pınar Aslan Koşar, Emine Nur Dinçer, Esma Selçuk, Öznur Kolay, İbrahim Hüseynov","doi":"10.1007/s12035-025-04764-1","DOIUrl":"10.1007/s12035-025-04764-1","url":null,"abstract":"Research on the tissue-protective effects of fluvoxamine (FLV), a selective serotonin reuptake inhibitor, rapidly expands. This study explores FLV's potential to protect against lipopolysaccharide (LPS)-induced neuroinflammation, a key factor in systemic inflammation-related neuronal damage. Four equal groups of thirty-two female Wistar Albino rats were created: FLV, LPS-FLV (50 mg/kg intraperitoneal), LPS (5 mg/kg intraperitoneal), and control. Both drugs were given in one dose on the same day. Tissues from the brain cortex, cerebellum, and hippocampus were taken for histopathology, immunohistochemistry, biochemistry, and genetic analysis. In the LPS group, histological examinations revealed hyperemia, edema, mild degeneration, neuronal death, and modest gliosis. Additionally, while apelin and total antioxidant status levels were reduced, greater levels of oxidative stress index, glial fibrillary acidic protein (GFAP), mammalian target of rapamycin (mTOR), and total oxidant status were noted. FLV treatment reversed all these findings. Genetic analyses revealed that LPS decreased sirtuin-1 (SIRT-1) and glutathione peroxidase 4 (GPX-4) while increasing high mobility group box protein 1 (HMGB-1). FLV treatment reversed all these parameters, and a significant result was obtained only with GPX-4. In this study, FLV treatment was shown to have anti-inflammatory and neuroprotective effects through various mechanisms on the brain cortex, cerebellum, and hippocampus tissues in addition to its antidepressant effects.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"7892-7902"},"PeriodicalIF":4.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12078383/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143425587","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}

引用次数: 0

Systematical Comparison Reveals Distinct Brain Transcriptomic Characteristics in Depression Models Induced by Gut Microbiota Dysbiosis and Chronic Stress. 系统比较揭示了肠道菌群失调和慢性应激诱导的抑郁模型中不同的脑转录组特征。

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2025-06-01 Epub Date: 2025-02-17 DOI: 10.1007/s12035-025-04766-z

Siwen Gui, Yiyun Liu, Juncai Pu, Dongfang Wang, Xiaogang Zhong, Weiyi Chen, Xiaopeng Chen, Yue Chen, Xiang Chen, Wei Tao, Peng Xie

{"title":"Systematical Comparison Reveals Distinct Brain Transcriptomic Characteristics in Depression Models Induced by Gut Microbiota Dysbiosis and Chronic Stress.","authors":"Siwen Gui, Yiyun Liu, Juncai Pu, Dongfang Wang, Xiaogang Zhong, Weiyi Chen, Xiaopeng Chen, Yue Chen, Xiang Chen, Wei Tao, Peng Xie","doi":"10.1007/s12035-025-04766-z","DOIUrl":"10.1007/s12035-025-04766-z","url":null,"abstract":"Major depressive disorder (MDD) is a devastating psychiatric illness with various etiologies. Both chronic stress and gut microbiome dysbiosis are implicated in the pathogenesis of MDD. However, limited research has been conducted to delineate the distinct effects of these two pathogenic factors on the brain transcriptome. We generated and compared transcriptomic features of the anterior cingulate cortex (ACC) from depressive-like mice induced by gut microbiome dysbiosis and canonical chronic stress paradigms, focusing on gene expression patterns and network characteristics. Data derived from MDD patients served as a reference standard to filter the molecular alterations associated with the disorder. Chronic stress induced a plethora of altered genes and biological functions associated with depression, prominently involving mitochondrial dysfunction. However, gut microbiota dysbiosis specifically regulated narrower range of genes and biological mechanisms, targeting aberrations in vesicular transport systems and perturbations of autophagy pathways. Network analysis revealed that hierarchical gene co-expression was specifically affected by gut microbiota dysbiosis rather than chronic stress. Further functional clustering analysis, along with the central distribution of inflammation-related differentially expressed genes, suggested an intricate interplay between disrupted autophagy processes, microglia-mediated inflammation, and synaptic dysfunctions in the network influenced by gut microbiota dysbiosis. Our findings reveal the distinctive transcriptomic alterations of brain shaped by gut microbiota and chronic stress in the development of MDD, contributing to a deeper understanding the heterogeneity of depression. Additionally, we provide a valuable data resource and bioinformatic analysis template for future studies.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"7957-7974"},"PeriodicalIF":4.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143441523","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}

引用次数: 0

Exploring Endothelial Cell Dysfunction's Impact on the Brain-Retina Microenvironment Connection: Molecular Mechanisms and Implications. 探索内皮细胞功能障碍对脑-视网膜微环境连接的影响：分子机制和意义。

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2025-06-01 Epub Date: 2025-02-04 DOI: 10.1007/s12035-025-04714-x

Wahid Shah, Yuxing Gong, Xin Qiao, Yaling Lu, Yufei Ding, Ziting Zhang, Yuan Gao

{"title":"Exploring Endothelial Cell Dysfunction's Impact on the Brain-Retina Microenvironment Connection: Molecular Mechanisms and Implications.","authors":"Wahid Shah, Yuxing Gong, Xin Qiao, Yaling Lu, Yufei Ding, Ziting Zhang, Yuan Gao","doi":"10.1007/s12035-025-04714-x","DOIUrl":"10.1007/s12035-025-04714-x","url":null,"abstract":"The intricate linking between the health of blood vessels and the functioning of neurons has attracted growing attention in the context of disorders that affect the neurological environment. Endothelial cells, forming the blood-brain barrier and blood-retinal barrier, play a fundamental role in maintaining the integrity of the brain-retina microenvironment connection. This review explores the molecular foundations of endothelial cell dysfunction and its implications for the brain-retina interaction. A comprehensive analysis of the complex factors contributing to endothelial dysfunction is presented, including oxidative stress, inflammation, reduced nitric oxide signaling, and disrupted vascular autoregulation. The significance of endothelial dysfunction extends to neurovascular coupling, synaptic plasticity, and trophic support. To our knowledge, there is currently no existing literature review addressing endothelial microvascular dysfunction and its interplay with the brain-retina microenvironment. The review also explains bidirectional communication between the brain and retina, highlighting how compromised endothelial function can disrupt this vital crosstalk and inhibit normal physiological processes. As neurodegenerative diseases frequently exhibit vascular involvement, a deeper comprehension of the interaction between endothelial cells and neural tissue holds promise for innovative therapeutic strategies. By targeting endothelial dysfunction, we may enhance our ability to preserve the intricate dynamics of the brain-retina microenvironment connection and ameliorate the progression of neurological disorders.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"7484-7505"},"PeriodicalIF":4.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189814","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}

引用次数: 0

Editorial: Are Mitochondrial Therapeutics the Next Disruptor in Molecular Healthcare? 社论：线粒体治疗学是分子医疗的下一个颠覆者吗？

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2025-06-01 DOI: 10.1007/s12035-023-03653-9

Benedict C Albensi

引用次数: 0

Pelargonium graveolens Attenuates Rotenone-Induced Parkinson's Disease in a Rat Model: Role of MAO-B Inhibition and In Silico Study. 天葵减轻鱼藤酮诱导的帕金森病大鼠模型：MAO-B抑制的作用和硅研究

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2025-06-01 Epub Date: 2025-02-08 DOI: 10.1007/s12035-025-04727-6

Rana M Merghany, Salma A El-Sawi, Asmaa F Aboul Naser, Mohamed A Salem, Shahira M Ezzat, Sherifa F A Moustafa, Meselhy R Meselhy

{"title":"Pelargonium graveolens Attenuates Rotenone-Induced Parkinson's Disease in a Rat Model: Role of MAO-B Inhibition and In Silico Study.","authors":"Rana M Merghany, Salma A El-Sawi, Asmaa F Aboul Naser, Mohamed A Salem, Shahira M Ezzat, Sherifa F A Moustafa, Meselhy R Meselhy","doi":"10.1007/s12035-025-04727-6","DOIUrl":"10.1007/s12035-025-04727-6","url":null,"abstract":"Parkinson's disease (PD), the second most common neurodegenerative condition, is primarily characterized by motor dysfunctions due to dopaminergic neuronal loss in the Substantia Nigra (SN), with oxidative stress playing a significant role in its progression. This study investigates the neuroprotective potential of Pelargonium graveolens (Thunb.) L'Hér leaves in a rotenone-induced PD rat model. The total ethanolic extract and its fractions, obtained via Diaion HP-20 column chromatography, were evaluated for monoamine oxidase-B (MAO-B) inhibition in vitro. The 50% methanol fraction (PG50) demonstrated the highest MAO-B inhibition (IC50 5.26 ± 0.12 µg/ml) compared to the reference drug selegiline (IC50 0.021 ± 0.003 µg/ml). In a rotenone-induced PD rat model, PG50 (100 mg/kg, p.o.) alleviated motor deficits (assessed via the wire hanging test), and restored norepinephrine, dopamine, and serotonin levels. PG50 and L-dopa reduced α-synuclein levels by 367.60% and 377.48%, respectively. Oxidative balance was restored with increased glutathione (23.12%) and decreased malondialdehyde (164.19%) in brain tissues. PG50 significantly reduced serum TNF-α (572.79%) and IL-6 (70.84%) levels, and improved succinate dehydrogenase (14.47%) and lactate dehydrogenase (7.74%) activities in brain tissues. Histopathological alterations in the SN were also ceased. UPLC-MS/MS analysis identified 61 metabolites, including 32 flavonoids, 13 phenolic acids, 7 coumarins, 5 phenolic glycosides, and 4 dicarboxylic acids, with in silico docking showing strong MAO-B binding by methoxylated flavonoids like methoxyluteolin dimethyl ether (docking score: - 8.0625 kcal/mol), surpassing that of safinamide (- 8.2615 kcal/mol). These findings suggest that P. graveolens holds promise as a neuroprotective agent against rotenone-induced PD.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"7664-7681"},"PeriodicalIF":4.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12078355/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143374371","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}

引用次数: 0

NF-κB Signaling Pathway in Rheumatoid Arthritis: Mechanisms and Therapeutic Potential. 类风湿关节炎中的 NF-κB 信号通路：机制与治疗潜力》。

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2025-06-01 Epub Date: 2024-11-19 DOI: 10.1007/s12035-024-04634-2

Haiyang Liao, Jianxiong Zheng, Jinyue Lu, Hai-Li Shen

{"title":"NF-κB Signaling Pathway in Rheumatoid Arthritis: Mechanisms and Therapeutic Potential.","authors":"Haiyang Liao, Jianxiong Zheng, Jinyue Lu, Hai-Li Shen","doi":"10.1007/s12035-024-04634-2","DOIUrl":"10.1007/s12035-024-04634-2","url":null,"abstract":"Rheumatoid arthritis (RA) is an autoimmune chronic inflammatory disease that imposes a heavy economic burden on patients and society. Bone and cartilage destruction is considered an important factor leading to RA, and inflammation, oxidative stress, and mitochondrial dysfunction are closely related to bone erosion and cartilage destruction in RA. Currently, there are limitations in the clinical treatment methods for RA, which urgently necessitates finding new effective treatments for patients. Nuclear transcription factor-κB (NF-κB) is a signaling transcription factor that is widely present in various cells. It plays an important role as a stress source in the cellular environment and regulates gene expression in processes such as immunity, inflammation, cell proliferation, and apoptosis. NF-κB has long been recognized as a pathogenic factor of RA, and its activation can exacerbate RA by promoting inflammation, oxidative stress, mitochondrial dysfunction, and bone destruction. Conversely, inhibiting the activity of the NF-κB pathway effectively inhibits these pathological processes, thereby alleviating RA. Therefore, NF-κB may be a potential therapeutic target for RA. This article describes the physiological structure of NF-κB and its important role in RA through the regulation of oxidative stress, inflammatory response, mitochondrial function, and bone destruction. Meanwhile, we also summarized the impact of NF-κB crosstalk with other signaling pathways on RA and the effect of related drugs or inhibitors targeting NF-κB on RA. The purpose of this article is to provide evidence for the role of NF-κB in RA and to emphasize its significant role in RA by elucidating the mechanisms, so as to provide a theoretical basis for targeting the NF-κB pathway as a treatment for RA.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"6998-7021"},"PeriodicalIF":4.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142667469","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}

引用次数: 0

A Novel m.1636A > G Variant in Mitochondrial TV Gene Might Cause New Phenotype of Mitochondrial Disease in a 2-Year Old Chinese Boy. 线粒体 TV 基因 m.1636A > G 变异可能导致 2 岁中国男孩线粒体病的新表型。

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2025-06-01 Epub Date: 2024-09-07 DOI: 10.1007/s12035-024-04472-2

Haiyan Yang, Victor Wei Zhang, Liang Ai, Liwen Wu

{"title":"A Novel m.1636A > G Variant in Mitochondrial TV Gene Might Cause New Phenotype of Mitochondrial Disease in a 2-Year Old Chinese Boy.","authors":"Haiyan Yang, Victor Wei Zhang, Liang Ai, Liwen Wu","doi":"10.1007/s12035-024-04472-2","DOIUrl":"10.1007/s12035-024-04472-2","url":null,"abstract":"Pathogenic variants of mitochondrial DNA (mtDNA) are associated with a large number of heterogeneous diseases involving multiple systems with which patients may present with a wide range of clinical phenotypes. Clinical data of the proband and his family members were gathered in a retrospective study. Whole-exome sequencing and full-length sequencing of the mitochondrial genome that was performed on peripheral blood, urine, and oral mucosa cells were applied for genetic analysis. In this study, we describe a 2-year-old Chinese boy with global developmental delay, Charcot-Marie-Tooth (CMT) disease, progressive myoclonic epilepsy, paroxysmal arrhythmia, and brain atrophy with elevated blood lactate levels. The clinical manifestations of the patient were improved after metabolic therapy, but the development regressed after infection. The molecular finding of whole-exome sequencing is unremarkable, but the mtDNA genome sequencing of the proband and his monther revealed a de novo novel heteroplasmic variant, m.1636A > G, located next to the highly conserved anticodon loop of tRNA Val (MT-TV) gene. Moreover, the higher levels of mutational load in urinary epithelial cells (19.05%) and oral mucosa cells (20.8%) were detected than that in blood (17.4%). Combined with the phenotypic and molecular genetics analysis of this family, this novel variation was currently considered to be a likely pathogenic variant. Our results added evidence that the de novo m.1636A > G variation in the highly conserved sequence of MT-TV appears to suggest a childhood-onset mitochondrial phenotype of a 2-year-old patient, thus broaden the genotypic interpretation of mitochondrial DNA-related disease.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"6764-6769"},"PeriodicalIF":4.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142145982","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}

引用次数: 0

Exosomes in Regulating miRNAs for Biomarkers of Neurodegenerative Disorders. 外泌体调节神经退行性疾病生物标志物mirna。

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2025-06-01 Epub Date: 2025-02-07 DOI: 10.1007/s12035-025-04733-8

Azhagu Madhavan Sivalingam, Darshitha D Sureshkumar

引用次数: 0

AMPK as a Therapeutic Target: Advancing Epilepsy Management Through Metabolic Modulation. AMPK作为治疗靶点：通过代谢调节推进癫痫管理。

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2025-06-01 Epub Date: 2025-02-12 DOI: 10.1007/s12035-025-04745-4

Maanvi Dhureja, Anjana Munshi, Puneet Kumar

{"title":"AMPK as a Therapeutic Target: Advancing Epilepsy Management Through Metabolic Modulation.","authors":"Maanvi Dhureja, Anjana Munshi, Puneet Kumar","doi":"10.1007/s12035-025-04745-4","DOIUrl":"10.1007/s12035-025-04745-4","url":null,"abstract":"Epilepsy is often marked by paroxysmal seizures that disrupt the brain's sensory, motor, and psychosocial functions. The underlying pathology is generally believed to involve an imbalance between excitatory and inhibitory neurotransmission. However, a less explored but significant contributor to epilepsy is the collapse of the brain's metabolic and bioenergetic systems. The breakdown of the brain's bioenergetic system leads to the activation of various detrimental downstream signaling cascades that ultimately result in oxidative stress, neuroinflammation, and reduced autophagic flux, all of which impair neuronal-glial communication and precipitate epileptic attacks. This highlights the pressing need for a therapeutic agent to address these complex challenges. Researchers have identified adenosine monophosphate kinase (AMPK) as a potential solution. AMPK acts as the body's primary stress sensor, activated in response to the deficiency of growth factors and nutrient starvation to restore energy homeostasis. AMPK activation also maintains the intricate communication between neurons and glial cells, preserving synaptic plasticity integrity, mitigating mitochondrial damage, and dampening inflammatory signaling cascades. Despite demonstrating significant efficacy in managing a range of peripheral and neurological disorders, the role of AMPK in neurotransmission and epilepsy remains unexplored. This review explores the multifaceted molecular roles of AMPK beyond its traditional metabolic regulatory functions, suggesting that targeting AMPK could provide a novel avenue for drug development in epilepsy treatment.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"7820-7834"},"PeriodicalIF":4.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143399528","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}

引用次数: 0