Molecular Neurobiology最新文献

{"title":"Melatonin Supplementation in Alzheimer's disease: The Potential Role in Neurogenesis.","authors":"Rasoul Ebrahimi, Ali Faramarzi, Shakiba Salarvandian, Reyhaneh Zarei, Moghadaseh Heidari, Fatemeh Salehian, Khadijeh Esmaeilpour","doi":"10.1007/s12035-025-05095-x","DOIUrl":"10.1007/s12035-025-05095-x","url":null,"abstract":"<p><p>Melatonin supplementation shows potential therapeutic effects in Alzheimer's disease (AD) by targeting impaired neurogenesis. Neurogenesis, the formation of new neurons after development, involves proliferation, migration, differentiation, and survival of neurons. Impaired neurogenesis is associated with AD, specifically in the subventricular zone (SVZ) and subgranular zone (SGZ), leading to hippocampal degeneration and memory impairment. Melatonin positively effects AD by regulating amyloid beta (Aβ)-induced neuroinflammation, reducing tau hyperphosphorylation, and enhancing adult neurogenesis through various signaling pathways. In addition, it has anti-apoptotic, antioxidative, and anti-inflammatory properties, suggesting its potential as a treatment option for AD progression. Furthermore, melatonin and sleep are closely linked, and an increase in sleep duration positively affects Aβ deposition. This review aims to examine the impact of AD pathologies on neurogenesis and explore the mechanisms by which melatonin may alleviate these pathologies, potentially promoting neurogenesis.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14987-15009"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144174153","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":"Ecdysterone and High-Intensity Interval Training Mitigate Alzheimer's Pathology in Rats: Impacts on Depression, Synaptic Plasticity, and Neuroinflammation.","authors":"Parsa Gholipour, Alireza Komaki, Hesam Parsa, Mahdi Ramezani","doi":"10.1007/s12035-025-05168-x","DOIUrl":"10.1007/s12035-025-05168-x","url":null,"abstract":"<p><p>The study focuses on the role of neuroinflammation and impaired synaptic plasticity in the progression of Alzheimer's disease caused by amyloid-beta accumulation. It examines the potential therapeutic effects of Ecdysterone, known for its anti-inflammatory and antioxidant properties, and high-intensity interval training, which may also support brain health. The primary goal is to assess how Ecdy and HIIT, alone or combined, influence depressive-like behavior, synaptic function, inflammation, and Aβ buildup in a rat model of AD. Ten days after Aβ administration, treatments began with Ecdy (10 mg/kg/day, orally) and/or HIIT, continuing for 8 weeks. Rats were tested for depression-like behavior using the forced swim test. Brain synaptic plasticity was measured through long-term potentiation at the perforant path-dentate gyrus synapse by analyzing population spike amplitude and fEPSP slope. Congo red staining was used to identify Aβ plaques in the brain, and neuroinflammatory markers were quantified in both the hippocampus and cerebral cortex. Aβ injection led to depression, impaired synaptic plasticity, increased inflammation, and Aβ buildup in the brain. While Ecdy and HIIT individually offered some protection, their combination was significantly more effective in improving depression, restoring synaptic function, reducing inflammation, and decreasing Aβ accumulation in both the hippocampus and cerebral cortex (0.05 > P). This data provides evidence that HIIT, accompanied by Ecdy, improves Aβ-induced depression-like behavior, which may be partly related to the amelioration of synaptic dysfunction, a decrease in neuroinflammation, and suppression of Aβ plaque formation.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"13933-13957"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575918","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":"Biomarker Discovery in Wilson's Disease-A Path Toward Improved Diagnosis and Management: A Comprehensive Review.","authors":"Marta Wolska, Zofia Wicik, Sara Ahmadova, Dagmara Mirowska-Guzel, Marek Postula, Anna Czlonkowska, Ceren Eyileten","doi":"10.1007/s12035-025-05143-6","DOIUrl":"10.1007/s12035-025-05143-6","url":null,"abstract":"<p><p>Wilson's disease (WD) is a rare autosomal recessive disorder characterized by defective copper metabolism, which leads to hepatic and neurological damage. The clinical presentation of WD varies significantly, often resulting in delayed diagnosis and an increased risk of irreversible complications. Current diagnostic tools, including biochemical assays, imaging techniques, and genetic testing, lack sufficient specificity and sensitivity, highlighting the need for novel biomarkers for early diagnosis and treatment monitoring. This review explores emerging biomarkers for both hepatic and neurological manifestations of WD, including blood-based molecular markers such as cytokines, proteases, oxidative stress indicators, inflammasomes, and gut microbiota signatures. Recent studies have identified neurofilament light chain (NfL), pentraxin 3 (PTX3), caspase-3/XIAP, and NLRP3 inflammasome activation as promising indicators of neurological impairment. Additionally, markers like soluble CD163 (sCD163) and apoptosis antigen 1 (APO-1) show potential for assessing hepatic dysfunction. Metabolomic and proteomic analyses further suggest distinct molecular profiles associated with different WD subtypes, while microRNA-based biomarkers offer novel insights into disease progression. Identifying and validating these biomarkers could enhance early diagnosis, predict neurological deterioration, and optimize treatment strategies, ultimately improving patient outcomes. Further research is needed to integrate these biomarkers into clinical practice and establish standardized protocols for their use in WD management.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"15189-15204"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511123/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144326287","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":"Gipc3 Mutation Might Cause Sensorineural Hearing Loss by Inhibiting Mitophagy in Inner Ear Hair Cells.","authors":"Xinxin Li, Jing Wang, Lin Shi, Liang Wang","doi":"10.1007/s12035-025-05178-9","DOIUrl":"10.1007/s12035-025-05178-9","url":null,"abstract":"<p><p>Sensorineural hearing loss (SNHL) has a high degree of genetic heterogeneity, with numerous mutated genes that contribute to deafness. GIPC3 gene is one of the mutated genes that can cause congenital hearing loss, which has been identified in recent years; however, the exact mechanism behind this condition remains unclear. Mitophagy is the process of selectively encapsulating and lysing damaged or dysfunctional mitochondria in order to prevent the accumulation of damaged mitochondria from damaging the cells and is of great importance in the maintenance of homeostasis in the inner ear. This paper aims to investigate the potential mechanism of sensorineural hearing loss brought on by Gipc3 mutations by observing the impact of Gipc3 expression on mitochondrial metabolism and autophagy in inner ear hair cells. In this study, The House Ear Institute Organ of Corti 1(HEI-OC1) cells and cochlear explants were cultured to change the expression level of Gipc3 by transfection, and the knockdown efficiency was examined by quantitative polymerase chain reaction (qPCR) and Western blot. Knockdown of Gipc3 inhibited cell viability and its proliferation ability. When tert-butyl hydroperoxide (t-BHP) was used to induce oxidative stress injury and knockdown of Gipc3, inner ear hair cells had a weakened ability to resist oxidative stress injury, mitochondrial metabolism was altered, and there was an accumulation of reactive oxygen species (ROS) and a reduction of mitochondrial membrane potential. Immunofluorescence and Western blot techniques demonstrated autophagy abnormalities in the mitophagy-related proteins LC3B and p62. Early endosome-dependent mitophagy is mediated by a PH domain and leucine zipper motif 1 (APPL1), and mitophagy is hampered by APPL1 deletion. We discovered that there is probably co-localization between Gipc3 and APPL1 by confocal microscopy imaging and that their trends show a positive association. In summary, Gipc3 mutations may lead to decreased mitochondrial function by inhibiting the APPL1-mediated mitophagy process. This may lead to a reduction in oxidative metabolism in hair cells, which is one potential mechanism via which Gipc3 mutations suppress mitophagy.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14050-14062"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626629","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":"The AMPK/GDF15 Axis: A Novel Target for the Neuroprotective Effects of Metformin in Ischemic Stroke.","authors":"Ghadah H Alshehri, Hayder M Al-Kuraishy, Bshra A Alsfouk, Ali I Al-Gareeb, Safaa A Faheem, Athanasios Alexiou, Marios Papadakis, Gaber El-Saber Batiha","doi":"10.1007/s12035-025-05126-7","DOIUrl":"10.1007/s12035-025-05126-7","url":null,"abstract":"<p><p>Metformin is an anti-diabetic drug used in the management of type 2 diabetes (T2D). Metformin has different pleiotropic effects, such as anti-inflammatory, antioxidant, antithrombotic, and vasculoprotective. Metformin has neuroprotective effects against neurodegenerative diseases and ischemic stroke. Conversely, metformin may exacerbate the pathogenesis of ischemic stroke. This controversial point may be related to the impact of metformin on the different signaling pathways, such as AMP-activated protein kinase (AMPK) and growth differentiation factor 15 (GDF-15). Many studies have reported the effect of metformin on ischemic stroke, with AMPK signaling only. However, little has been explored about the impact of metformin on the GDF-15 signaling in ischemic stroke. Accordingly, this review aims to discuss the role of metformin in the neuropathology of ischemic stroke regarding the AMPK and GDF-15 signaling pathways.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"15149-15163"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511219/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144248796","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":"Mechanisms of Senegenin in Regulating Oxidative Stress and Mitochondria Damage for Neuroprotection in Insomnia: Evidence from In Vivo and In Vitro Models.","authors":"Honglin Jia, Zhengting Liang, Deqi Yan, Xu Chen, Ruining Liang, Jinhong Wu, Xingping Zhang","doi":"10.1007/s12035-025-05170-3","DOIUrl":"10.1007/s12035-025-05170-3","url":null,"abstract":"<p><p>Insomnia is a common sleep disorder worldwide, and oxidative stress and mitochondrial damage are closely related to insomnia. This study aimed to investigate the mechanism by which senegenin exerts neuroprotective effects in regulating oxidative stress and mitochondrial damage in insomnia. In vivo, EEG/EMG analysis confirmed the successful establishment of insomnia rat models; Nissl and HE staining and electron microscopy were used to evaluate the pathological changes of neurons and mitochondria in rat brain tissue. The expression of oxidative stress and sleep factors was assessed. In vitro, an oxidative damage cell model was established to measure oxidative stress-related parameters; the protective concentration of senegenin against oxidative damage was determined using the CCK-8 assay, and the effects of senegenin on the expression of Keap1/Nrf2 and PINK1/Parkin, key signaling pathways involved in oxidative stress and mitochondrial damage, were analyzed. During insomnia, wake is prolonged, and NREM and REM are shortened; learning memory and exploration behavior are impaired, oxidative stress factor expression is changed, and mitochondria are damaged. Brain tissue from insomnia rats showed decreased BDNF, 5-HT1A, GABA-T, and GAD and increased expression of 5-HT2A and Glu. Keap1, PINK1, Parkin, and LC3 expression increased and Nrf2, NQO1, HO-1, and p62 expression decreased in oxidatively injured cells. Senegenin showed a dose-response regulatory effect after the intervention. Senegenin may exert neuroprotective effects in insomnia by improving oxidative stress and mitochondrial damage.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"13917-13932"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511245/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560529","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":"Ceramides may Play a Central Role in the Pathogenesis of Alzheimer's Disease: a Review of Evidence and Horizons for Discovery.","authors":"Hans O Kalkman, Lukasz Smigielski","doi":"10.1007/s12035-025-04989-0","DOIUrl":"10.1007/s12035-025-04989-0","url":null,"abstract":"<p><p>While several hypotheses have been proposed to explain the underlying mechanisms of Alzheimer's disease, none have been entirely satisfactory. Both genetic and non-genetic risk factors, such as infections, metabolic disorders and psychological stress, contribute to this debilitating disease. Multiple lines of evidence indicate that ceramides may be central to the pathogenesis of Alzheimer's disease. Tumor necrosis factor-α, saturated fatty acids and cortisol elevate the brain levels of ceramides, while genetic risk factors, such as mutations in APP, presenilin, TREM2 and APOE ε4, also elevate ceramide synthesis. Importantly, ceramides displace sphingomyelin and cholesterol from lipid raft-like membrane patches that connect the endoplasmic reticulum and mitochondria, disturbing mitochondrial oxidative phosphorylation and energy production. As a consequence, the flattening of lipid rafts alters the function of γ-secretase, leading to increased production of Aβ₄₂. Moreover, ceramides inhibit the insulin-signaling cascade via at least three mechanisms, resulting in the activation of glycogen synthase kinase-3 β. Activation of this kinase has multiple consequences, as it further deteriorates insulin resistance, promotes the transcription of BACE1, causes hyperphosphorylation of tau and inhibits the transcription factor Nrf2. Functional Nrf2 prevents apoptosis, mediates anti-inflammatory activity and improves blood-brain barrier function. Thus, various seemingly unrelated Alzheimer's disease risk factors converge on ceramide production, whereas the elevated levels of ceramides give rise to the well-known pathological features of Alzheimer's disease. Understanding and targeting these mechanisms may provide a promising foundation for the development of novel preventive and therapeutic strategies.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14424-14441"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511167/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144008461","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":"Decoding the Gut Microbiota in Multiple Sclerosis Using Nanopore Long-Read Sequencing: Insights into Disease Severity and Subtypes.","authors":"Ameera Saeed Alshinnawy, Elham A Badiea, Mahmoud Saad Swelam, Ahmed A Sayed, Mohamed R Mohamed","doi":"10.1007/s12035-025-05194-9","DOIUrl":"10.1007/s12035-025-05194-9","url":null,"abstract":"<p><p>Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS), characterized by neuroinflammation and neurodegeneration. Emerging evidence links gut microbiota dysbiosis to immune dysregulation and MS progression. While extensive research has been conducted in Western populations, region-specific studies are needed to assess the influence of local genetic and environmental factors. This study investigates gut microbiota alterations in Egyptian MS patients using Oxford Nanopore sequencing to identify microbial signatures associated with disease progression. Fecal samples from 33 newly diagnosed MS patients (20 with relapsing-remitting MS [RRM] and 13 with Progressive MS [PMS]) and 10 healthy controls were analyzed using long-read Oxford Nanopore sequencing of the full 16S rRNA gene. MS patients exhibited increased microbial richness but reduced evenness, with distinct gut microbiome profiles. Progressive MS was characterized by an abundance of pro-inflammatory bacteria (e.g., Enterococcus faecium and Romboutsia timonensis) and a depletion of short-chain fatty acid (SCFA)-producing species (Ruminococcus bromii and Faecalibacterium duncaniae), potentially contributing to heightened neuroinflammation and disease progression. Relapsing MS exhibited microbial shifts indicative of immune dysregulation, including increased Clostridium saudiense and decreased levels of the gut-protective Faecalibacterium butyricigenerans. Functional analysis linked these microbial alterations to oxidative stress, neurotransmitter imbalance, and suppressed lipid and carbohydrate metabolism. These findings underscore the role of gut microbiota dysbiosis in MS pathogenesis and, by focusing on an underexplored Egyptian cohort, highlight region-specific microbial shifts that may inform targeted therapeutic strategies for both Progressive and Relapsing forms of MS.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14245-14260"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511234/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144659671","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":"Exploring Exosome-Based Approaches for Early Diagnosis and Treatment of Neurodegenerative Diseases.","authors":"Vibhav Varshney, Baneen C Gabble, Ashok Kumar Bishoyi, Pooja Varma, Sarraa Ahmad Qahtan, Aditya Kashyap, Rajashree Panigrahi, Deepak Nathiya, Ashish Singh Chauhan","doi":"10.1007/s12035-025-05026-w","DOIUrl":"10.1007/s12035-025-05026-w","url":null,"abstract":"<p><p>Neurodegenerative diseases (NDs), like Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and Amyotrophic Lateral Sclerosis (ALS), present an increasingly significant global health burden, primarily due to the lack of effective early diagnostic tools and treatments. Exosomes-nano-sized extracellular vesicles secreted by nearly all cell types-have emerged as promising candidates for both biomarkers and therapeutic agents in NDs. This review examines the biogenesis, molecular composition, and diverse functions of exosomes in NDs. Exosomes play a crucial role in mediating intercellular communication. They are capable of reflecting the biochemical state of their parent cells and have the ability to cross the blood-brain barrier (BBB). In doing so, they facilitate the propagation of pathological proteins, such as amyloid-beta (Aβ), tau, and alpha-synuclein (α-syn), while also enabling the targeted delivery of neuroprotective compounds. Recent advancements in exosome isolation and engineering have opened up new possibilities for diagnostic and therapeutic strategies. These range from the discovery of non-invasive biomarkers to innovative approaches in gene therapy and drug delivery systems. However, challenges related to standardization, safety, and long-term effects must be addressed before exosomes can be translated into clinical applications. This review highlights both the promising potential and the obstacles that must be overcome to leverage exosomes in the treatment of NDs and the transformation of personalized medicine.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14683-14705"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971912","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":"Emerging Roles of Meningeal Lymphatic Vessels in Ischemic Stroke.","authors":"Richard Simon Machado, Khiany Mathias, Larissa Joaquim, Maiara de Aguiar da Costa, Anita Tiscoski, Cinara Ludvig Gonçalves, Gislaine Tezza Rezin, Fabricia Petronilho","doi":"10.1007/s12035-025-04983-6","DOIUrl":"10.1007/s12035-025-04983-6","url":null,"abstract":"<p><p>This review highlights the emerging relevance of meningeal lymphatic vessels (MLVs) in the context of ischemic stroke, challenging the conventional view of a privileged immunological central nervous system. MLVs facilitate immunological surveillance by modulating the entry of peripheral immune cells into the meningeal compartment, a process not impeded by the blood-brain barrier. In ischemic stroke, these vessels play a crucial role in the neuroinflammatory cascade, contributing to immune responses by draining antigens and signals to cervical lymph nodes. Their involvement extends to potential contributions to resolving ischemia-induced cerebral edema, impacting fluid homeostasis. The dynamic interaction among MLVs, neuroinflammation, and fluid dynamics suggests promising therapeutic approaches. Targeting these vessels for immunomodulation, fluid drainage, and preserving blood-brain barrier integrity emerges as an innovative approach to improve ischemic stroke outcomes. However, successful clinical translation awaits further exploration of the therapeutic potential of these vessels. The multifaceted contributions of MLVs provide a compelling rationale for ongoing research, aiming to fully harness their therapeutic impact in ischemic stroke management.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14442-14458"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143992654","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}