Cellular and Molecular Neurobiology最新文献_第2页

Targeting Neuroinflammation in Preterm White Matter Injury: Therapeutic Potential of Mesenchymal Stem Cell-Derived Exosomes.

IF 3.6 4区医学

Cellular and Molecular Neurobiology Pub Date : 2025-03-12 DOI: 10.1007/s10571-025-01540-6

Xinling Zhang, Yuhang Zhang, Xirui Peng, Luxiang Yang, Jingwen Miao, Yuyang Yue, Yong Wang, Xiaoyang Wang, Changlian Zhu, Juan Song

{"title":"Targeting Neuroinflammation in Preterm White Matter Injury: Therapeutic Potential of Mesenchymal Stem Cell-Derived Exosomes.","authors":"Xinling Zhang, Yuhang Zhang, Xirui Peng, Luxiang Yang, Jingwen Miao, Yuyang Yue, Yong Wang, Xiaoyang Wang, Changlian Zhu, Juan Song","doi":"10.1007/s10571-025-01540-6","DOIUrl":"10.1007/s10571-025-01540-6","url":null,"abstract":"Neuroinflammation is a key factor in the development of preterm white matter injury (PWMI), leading to glial cell dysfunction, arrest of oligodendrocyte maturation, and long-term neurological damage. As a potential therapeutic strategy, mesenchymal stem cells (MSCs) exhibit significant immunomodulatory and regenerative potential. Recent studies suggest that the primary mechanism of MSC action is their paracrine effects, particularly mediated by extracellular vesicles, with MSC-derived exosomes (MSC-Exos) being the key mediators. MSC-Exos, enriched with lipids, proteins, and nucleic acids, regulate neuroinflammation by modulating glial cell activity and influencing signaling pathways associated with inflammation and repair. Preclinical evidence has indicated that MSC-Exos can suppress the activation of microglia and astrocytes, promote oligodendrocyte maturation, and enhance myelination, highlighting their potential as a cell-free treatment for PWMI. However, there are a paucity of comprehensive reviews on how MSC-Exos regulate neuroinflammation in PWMI through specific signaling pathways. This review aims to summarize the key signaling pathways through which MSC-Exos modulate neuroinflammation in PWMI and discuss the challenges associated with the clinical application of MSC-Exos-based therapies.","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"23"},"PeriodicalIF":3.6,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11903990/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Beyond Diabetes: Semaglutide's Role in Modulating Mood Disorders through Neuroinflammation Pathways.

IF 3.6 4区医学

Cellular and Molecular Neurobiology Pub Date : 2025-03-10 DOI: 10.1007/s10571-025-01534-4

Iwona Piątkowska-Chmiel, Katarzyna Wicha-Komsta, Kamil Pawłowski, Aleksandra Syrytczyk, Tomasz Kocki, Jarosław Dudka, Mariola Herbet

{"title":"Beyond Diabetes: Semaglutide's Role in Modulating Mood Disorders through Neuroinflammation Pathways.","authors":"Iwona Piątkowska-Chmiel, Katarzyna Wicha-Komsta, Kamil Pawłowski, Aleksandra Syrytczyk, Tomasz Kocki, Jarosław Dudka, Mariola Herbet","doi":"10.1007/s10571-025-01534-4","DOIUrl":"10.1007/s10571-025-01534-4","url":null,"abstract":"Diabetes and mood disorders are intricately interconnected, with each condition elevating the risk of the other. This bidirectional relationship, further exacerbated by neuroinflammation, fosters an environment conducive to the development of anxiety and depression. Glucagon-like peptide-1 receptor agonists, such as semaglutide, offer promising therapeutic options that not only target type 2 diabetes but also can positively influence mood. Our study's primary goal was to evaluate the effectiveness of semaglutide, in mitigating anxiety and depression within an animal model of diabetes. The neuroprotective properties of semaglutide were evaluated by examining its influence on the kynurenine pathway and neurobiological markers (GFAP, NEFL, NSE, and GAL3) in the perfrontal cortex, selected for its key role in cognitive function and emotional regulation, impaired in diabetes and mood disorders. Additionally, we examined semaglutide's impact on peripheral inflammation and stress parameters to elucidate its role in modulating systemic inflammatory responses linked to mood disorders. Additionally, we conducted behavioral assessments to better understand how semaglutide influences anxiety and depression-related behaviors in diabetic mice. Semaglutide therapy significantly improved behavioral patterns and neurochemical markers in diabetic mice. The frequency of administration significantly influenced the outcomes, whereas the dosage appeared to have a limited impact. Here we show that semaglutide expands its therapeutic potential beyond diabetes, significantly influencing mood disorders through neuroinflammatory pathways. Semaglutide has the potential to be a key element in formulating integrated treatment strategies that address both metabolic health and mental well-being, ultimately enhancing the quality of life for individuals navigating these interrelated challenges.","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"22"},"PeriodicalIF":3.6,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11891103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

LncRNAs Orchestrating Neuroinflammation: A Comprehensive Review.

IF 3.6 4区医学

Cellular and Molecular Neurobiology Pub Date : 2025-03-08 DOI: 10.1007/s10571-025-01538-0

Arash Esmaeili, Niloufar Yazdanpanah, Nima Rezaei

{"title":"LncRNAs Orchestrating Neuroinflammation: A Comprehensive Review.","authors":"Arash Esmaeili, Niloufar Yazdanpanah, Nima Rezaei","doi":"10.1007/s10571-025-01538-0","DOIUrl":"10.1007/s10571-025-01538-0","url":null,"abstract":"CNS diseases account for a major part of the comorbidity and mortality of the human population; moreover, neuroinflammation has become an indication for different CNS diseases, for instance, Parkinson's and Alzheimer's disease. Microglia and astrocytes are the two main glial cells that can be found in the CNS. Each of these plays an important role in mediating immune responses like inflammation. There are many studies suggesting the role of LncRNAs in mediating neuroinflammation. Indeed, LncRNAs orchestrate neuroinflammation through various mechanisms, namely miRNA sponge, and transcriptional activation/inhibition. In addition, LncRNAs regulate different downstream pathways like NF-κB, and PI3K/AKT. In this study, we gathered the existing studies regarding the mechanisms of action of LncRNAs in the pathogenesis of different CNS diseases like neurodegenerative diseases and traumatic injuries through regulating neuroinflammation. We aim to elaborate on the regulatory roles of LncRNAs in neuroinflammation and bring a more profound understanding of the etiology of CNS diseases in terms of neuroinflammation.","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"21"},"PeriodicalIF":3.6,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890384/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143582210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Single-Cell Analysis of Sex and Gender Differences in the Human Brain During Development and Disease.

IF 3.6 4区医学

Cellular and Molecular Neurobiology Pub Date : 2025-02-27 DOI: 10.1007/s10571-025-01536-2

Aura Zelco, Anagha Joshi

{"title":"Single-Cell Analysis of Sex and Gender Differences in the Human Brain During Development and Disease.","authors":"Aura Zelco, Anagha Joshi","doi":"10.1007/s10571-025-01536-2","DOIUrl":"10.1007/s10571-025-01536-2","url":null,"abstract":"Sex and gender (SG) differences in the human brain are of interest to society and science as numerous processes are impacted by them, including brain development, behavior, and diseases. By collecting publicly available single-cell data from the in-utero to elderly age in healthy, Alzheimer's disease and multiple sclerosis samples, we identified and characterized SG-biased genes in ten brain cell types across 9 age and disease groups. Sex and gender differences in the transcriptome were present throughout the lifespan and across all cell types. Although there was limited overlap among SG-biased genes across different age and disease groups, we observed significant functional overlap. Female-biased genes are consistently enriched for brain-related processes, while male-biased genes are enriched for metabolic pathways. Additionally, mitochondrial genes showed a consistent female bias across cell types. We also found that androgen response elements (not estrogen) were significantly enriched in both male- and female-biased genes, and thymosin hormone targets being consistently enriched only in male-biased genes. We systematically characterised SG differences in brain development and brain-related disorders at a single-cell level, by analysing a total of publicly available 419,885 single nuclei from 161 human brain samples (72 females, 89 males). The significant enrichment of androgen (not estrogen) response elements in both male- and female-biased genes suggests that androgens are important regulators likely establishing these SG differences. Finally, we provide full characterization of SG-biased genes at different thresholds for the scientific community as a web resource.","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"20"},"PeriodicalIF":3.6,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11868228/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Organochlorine Pesticides and Epigenetic Alterations in Brain Cancer.

IF 3.6 4区医学

Cellular and Molecular Neurobiology Pub Date : 2025-02-09 DOI: 10.1007/s10571-025-01535-3

Fatemeh Yousefi, Gholamreza Asadikaram, Saeid Karamouzian, Moslem Abolhassani, Hossein Pourghadamyari, Vahid Moazed

{"title":"Organochlorine Pesticides and Epigenetic Alterations in Brain Cancer.","authors":"Fatemeh Yousefi, Gholamreza Asadikaram, Saeid Karamouzian, Moslem Abolhassani, Hossein Pourghadamyari, Vahid Moazed","doi":"10.1007/s10571-025-01535-3","DOIUrl":"10.1007/s10571-025-01535-3","url":null,"abstract":"Epigenetic alterations have emerged as critical factors in the pathogenesis of brain cancer, particularly gliomas. This article explores the impact of organochlorine pesticides (OCPs) on the hypermethylation of key tumor suppressor genes, and some histone modifications in primary brain tumor (PBT) patients. This study involved 73 patients diagnosed with PBT and 15 non-cancerous brain tissue samples as contol. DNA extracted from tumor specimens was used to evaluate the methylation status of tumor suppressor genes, P16 and RRP22, using the methylation-specific PCR (MSP) technique and four histone marks (H4K16ac, H3K9ac, H4K20me3, and H3k4me2) to investigate by western blotting. The results of MSP revealed the methylation of RRP22 and P16 promoter regions and western blot analysis demonstrated significantly low levels of H3K9ac, H4K20me3, and H3K4me2 in PBT patients in comparison with the controls. The results of regression analysis revealed direct and significant correlations between serum OCPs concentration and methylation of RRP22 and P16. Furthermore, a direct and significant association was observed between hypomethylation of histones H3K4 and H4K20, as well as hypoacetylation of H3K9, with OCPs levels. This study revealed that epigenetic modifications play a significant role in the development of brain tumors, with OCPs identified as key contributors to these changes. Our research indicated that in patients with PBT, hypermethylation of the RRP22 and P16 gene and histone modifications correlates directly and significantly with the levels of OCPs found in their serum.","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"19"},"PeriodicalIF":3.6,"publicationDate":"2025-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11807917/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143373888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Differential Neuronal Activation of Nociceptive Pathways in Neuropathic Pain After Spinal Cord Injury.

IF 3.6 4区医学

Cellular and Molecular Neurobiology Pub Date : 2025-01-30 DOI: 10.1007/s10571-025-01532-6

Ziyu He, Jun Zhang, Jia Xu, Yu Wang, Xiaolong Zheng, Wei Wang

{"title":"Differential Neuronal Activation of Nociceptive Pathways in Neuropathic Pain After Spinal Cord Injury.","authors":"Ziyu He, Jun Zhang, Jia Xu, Yu Wang, Xiaolong Zheng, Wei Wang","doi":"10.1007/s10571-025-01532-6","DOIUrl":"10.1007/s10571-025-01532-6","url":null,"abstract":"Neuropathic pain, a prevalent complication following spinal cord injury (SCI), severely impairs the life quality of patients. No ideal treatment exists due to incomplete knowledge on underlying neural processes. To explore the SCI-induced effect on nociceptive circuits, the protein expression of c-Fos was analyzed as an indicator of neuronal activation in a rat contusion model exhibiting below-level pain. Additional stimuli were delivered to mimic the different peripheral sensory inputs in daily life. Following noxious rather than innocuous or no stimulation, a greater number of spinal dorsal horn (DH) neurons were activated after SCI, mainly in the deep DH. SCI facilitated the activation of excitatory but not inhibitory DH neurons. Moreover, excitatory interneurons expressing protein kinase C gamma (PKCγ) in laminae II-III, which are known to play a role in mechanical allodynia after peripheral nerve injury, responded in larger amounts to both innocuous and noxious stimulation following SCI. Accordingly, more spinal projection neurons in lamina I were activated. Within supraspinal nuclei processing pain, differentially enhanced activation in response to noxious stimulation was detected after SCI, with a significant increase in the locus coeruleus and medial thalamus, a slight increase in the periaqueductal gray and dorsal raphe, and no change in the lateral parabrachial nucleus or primary sensory cortex. These findings indicated differential hyperexcitability along the sensory neuroaxis following SCI, with a particular emphasis on the involvement of specific neuron subtypes, such as spinal PKCγ interneurons and locus coeruleus noradrenergic neurons, which may serve as crucial targets for potential therapies.","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"18"},"PeriodicalIF":3.6,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11782389/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143064063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Correction: Myosin IIA Regulated Tight Junction in Oxygen Glucose-Deprived Brain Endothelial Cells Via Activation of TLR4/PI3K/Akt/JNK1/2/14-3-3ε/NF-κB/MMP9 Signal Transduction Pathway.

IF 3.6 4区医学

Cellular and Molecular Neurobiology Pub Date : 2025-01-28 DOI: 10.1007/s10571-025-01531-7

Yanni Lv, Wen Liu, Zhaohui Ruan, Zixuan Xu, Longsheng Fu

引用次数: 0

Correction: Docosahexaenoic Acid Alleviates Oxidative Stress-Based Apoptosis Via Improving Mitochondrial Dynamics in Early Brain Injury After Subarachnoid Hemorrhage.

IF 3.6 4区医学

Cellular and Molecular Neurobiology Pub Date : 2025-01-25 DOI: 10.1007/s10571-025-01530-8

Tongyu Zhang, Pei Wu, John H Zhang, Yuchen Li, Shancai Xu, Chunlei Wang, Ligang Wang, Guang Zhang, Jiaxing Dai, Shiyi Zhu, Yao Liu, Binbing Liu, Cesar Reis, Huaizhang Shi

引用次数: 0

AMPA Receptors in Synaptic Plasticity, Memory Function, and Brain Diseases. AMPA受体在突触可塑性、记忆功能和脑部疾病中的作用。

IF 3.6 4区医学

Cellular and Molecular Neurobiology Pub Date : 2025-01-22 DOI: 10.1007/s10571-024-01529-7

Cristina A Muñoz de León-López, Marta Carretero-Rey, Zafar U Khan

{"title":"AMPA Receptors in Synaptic Plasticity, Memory Function, and Brain Diseases.","authors":"Cristina A Muñoz de León-López, Marta Carretero-Rey, Zafar U Khan","doi":"10.1007/s10571-024-01529-7","DOIUrl":"10.1007/s10571-024-01529-7","url":null,"abstract":"Tetrameric AMPA-type ionotropic glutamate receptors are primary transducers of fast excitatory synaptic transmission in the central nervous system, and their properties and abundance at the synaptic surface are crucial determinants of synaptic efficacy in neuronal communication across the brain. The induction of long-term potentiation (LTP) leads to the insertion of GluA1-containing AMPA receptors at the synaptic surface, whereas during long-term depression (LTD), these receptors are internalized into the cytoplasm of the spine. Disruptions in the trafficking of AMPA receptors to and from the synaptic surface attenuate both forms of synaptic plasticity. Homeostatic scaling up and scaling down, which are additional types of plasticity similar to LTP and LTD, are also regulated by the insertion and removal of GluA1-containing AMPA receptors from the synaptic surface. The trafficking of AMPA receptors is an intricate process assisted by various proteins. Furthermore, AMPA receptors are critical for the formation and consolidation of various types of memory, and alterations in their function are intimately associated with cognitive dysfunction in aging and several neurological and psychiatric diseases. In this review, we will provide an overview of the current understanding of how AMPA receptors regulate various forms of synaptic plasticity, their contribution to memory functions, and their role in aging and brain diseases.","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"14"},"PeriodicalIF":3.6,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11754374/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Genetically Predicted Leucine Level Mediates Association Between CD4/CD8br T Lymphocytes and Insomnia. 基因预测的亮氨酸水平介导CD4/CD8br T淋巴细胞与失眠的关系

IF 3.6 4区医学

Cellular and Molecular Neurobiology Pub Date : 2025-01-22 DOI: 10.1007/s10571-025-01533-5

Sumei Luo, Jianyin Yin, Jie Zhang, Pan Li, Tao Wen, Ke Li, Jing Tang, Xiaohong Wang, Aiyuan Li, Liang Chen

{"title":"Genetically Predicted Leucine Level Mediates Association Between CD4/CD8br T Lymphocytes and Insomnia.","authors":"Sumei Luo, Jianyin Yin, Jie Zhang, Pan Li, Tao Wen, Ke Li, Jing Tang, Xiaohong Wang, Aiyuan Li, Liang Chen","doi":"10.1007/s10571-025-01533-5","DOIUrl":"10.1007/s10571-025-01533-5","url":null,"abstract":"Immune and metabolic factors play an important role in the onset and development of insomnia. This study aimed to investigate the causal relationship between insomnia and immune cells and metabolites. Data for 731 immune cell phenotypes, 1400 metabolites, and insomnia in this study were obtained from the GWAS open-access database. Two-way Mendelian randomization was used to (1) detect the causal relationship between immune cells and insomnia and (2) identify potential mediating metabolites. Mendelian randomization analysis identified eight immune cell phenotypes with a causal relationship to insomnia, and two immune cell phenotypes were protective factors for insomnia, namely CD8br %T cells and CD80 on CD62L + myeloid dendritic cells. The other six immune cell phenotypes were risk factors for insomnia, i.e., CD4/CD8br, CD16-CD56 on NKT, CCR2 on myeloid dendritic cells, CD40 on monocytes, CD38 on CD3-CD19-, and CD25 on CD45RA + CD4 not Treg. Further Mendelian randomization revealed 11 metabolites that were causally related to insomnia. Five metabolites were protective factors for insomnia, i.e., 3-hydroxy-3-methylglutarate, cholate, dodecanedioate, N-formylmethionine, and x-26054. Six metabolites were risk factors for insomnia, 3-amino-2-piperidone, 6-oxopiperdine-2-carboxylate, caffeine to theophylline ratio, leucine, maltose, and x-24736. In addition, our analysis showed that leucine mediated the association between CD4/CD8br and insomnia. From genetic information, we confirmed the causal relationship between insomnia, eight immune cell phenotypes, and eleven metabolite levels. Notably, we found a relationship between leucine-mediated CD4/CD8br and insomnia, providing evidence supporting the causal relationship between immune cell and insomnia, with plasma metabolites serving as mediators.","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"15"},"PeriodicalIF":3.6,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11754360/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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