Cellular and Molecular Neurobiology最新文献

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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":"<p><p>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.</p>","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":"<p><p>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.</p>","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
Aging and MPTP Sensitivity Depend on Molecular and Ultrastructural Signatures of Astroglia and Microglia in Mice Substantia Nigra. 衰老和MPTP敏感性取决于小鼠黑质星形胶质细胞和小胶质细胞的分子和超微结构特征。
IF 3.6 4区 医学
Cellular and Molecular Neurobiology Pub Date : 2025-01-20 DOI: 10.1007/s10571-024-01528-8
P L Abhilash, Upasna Bharti, Santhosh Kumar Rashmi, Mariamma Philip, T R Raju, Bindu M Kutty, B K Chandrasekhar Sagar, Phalguni Anand Alladi
{"title":"Aging and MPTP Sensitivity Depend on Molecular and Ultrastructural Signatures of Astroglia and Microglia in Mice Substantia Nigra.","authors":"P L Abhilash, Upasna Bharti, Santhosh Kumar Rashmi, Mariamma Philip, T R Raju, Bindu M Kutty, B K Chandrasekhar Sagar, Phalguni Anand Alladi","doi":"10.1007/s10571-024-01528-8","DOIUrl":"10.1007/s10571-024-01528-8","url":null,"abstract":"<p><p>Both astroglia and microglia show region-specific distribution in CNS and often maladapt to age-associated alterations within their niche. Studies on autopsied substantia nigra (SN) of Parkinson's disease (PD) patients and experimental models propose gliosis as a trigger for neuronal loss. Epidemiological studies propose an ethnic bias in PD prevalence, since Caucasians are more susceptible than non-whites. Similarly, different mice strains are variably sensitive to MPTP. We had earlier likened divergent MPTP sensitivity of C57BL/6 J and CD-1 mice with differential susceptibility to PD, based on the numbers of SN neurons. We examined whether the variability was incumbent to inter-strain differences in glial features of male C57BL/6 J and CD-1 mice. Stereological counts showed relatively more microglia and fewer astrocytes in the SN of normal C57BL/6 J mice, suggesting persistence of an immune-vigilant state. MPTP-induced microgliosis and astrogliosis in both strains suggest their involvement in pathogenesis. ELISA of pro-inflammatory cytokines in the ventral-midbrain revealed augmentation of TNF-α and IL-6 at middle age in both strains that reduced at old age, suggesting middle age as a critical, inflamm-aging-associated time point. TNF-α levels were high in C57BL/6 J, through aging and post-MPTP, while IL-6 and IL-1β were upregulated at old age. CD-1 had higher levels of anti-inflammatory cytokine TGF-β. MPTP challenge caused upregulation of enzymes MAO-A, MAO-B, and iNOS in both strains. Post-MPTP enhancement in fractalkine and hemeoxygenase-1 may be neuron-associated compensatory signals. Ultrastructural observations of elongated astroglial/microglial mitochondria vis-à-vis the shrunken ones in neurons suggest a scale-up of their functions with neurotoxic consequences. Thus, astroglia and microglia may modulate aging and PD susceptibility.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"13"},"PeriodicalIF":3.6,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11753320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000764","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: Sevoflurane Induces Learning and Memory Impairment in Young Mice Through a Reduction in Neuronal Glucose Transporter 3. 更正:七氟醚通过减少神经元葡萄糖转运蛋白3诱导幼鼠学习和记忆障碍。
IF 3.6 4区 医学
Cellular and Molecular Neurobiology Pub Date : 2025-01-16 DOI: 10.1007/s10571-024-01520-2
Jinpiao Zhu, Zongze Zhang, Junke Jia, Lirong Wang, Qiuyue Yang, Yanlin Wang, Chang Chen
{"title":"Correction: Sevoflurane Induces Learning and Memory Impairment in Young Mice Through a Reduction in Neuronal Glucose Transporter 3.","authors":"Jinpiao Zhu, Zongze Zhang, Junke Jia, Lirong Wang, Qiuyue Yang, Yanlin Wang, Chang Chen","doi":"10.1007/s10571-024-01520-2","DOIUrl":"https://doi.org/10.1007/s10571-024-01520-2","url":null,"abstract":"","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"12"},"PeriodicalIF":3.6,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11739275/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000768","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: Expression of CGRP in the Trigeminal Ganglion and Its Effect on the Polarization of Macrophages in Rats with Temporomandibular Arthritis. 修正:CGRP在三叉神经节的表达及其对颞下颌关节炎大鼠巨噬细胞极化的影响。
IF 3.6 4区 医学
Cellular and Molecular Neurobiology Pub Date : 2025-01-09 DOI: 10.1007/s10571-024-01527-9
Junli Tao, Xiaohui Wang, Jie Xu
{"title":"Correction: Expression of CGRP in the Trigeminal Ganglion and Its Effect on the Polarization of Macrophages in Rats with Temporomandibular Arthritis.","authors":"Junli Tao, Xiaohui Wang, Jie Xu","doi":"10.1007/s10571-024-01527-9","DOIUrl":"10.1007/s10571-024-01527-9","url":null,"abstract":"","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"11"},"PeriodicalIF":3.6,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11717830/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142945430","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
A Focal Traumatic Injury to the Neonatal Rodent Spinal Cord Causes an Immediate and Massive Spreading Depolarization Sustained by Chloride Ions, with Transient Network Dysfunction. 幼鼠脊髓局灶性创伤损伤引起氯离子维持的立即和大量扩张性去极化,并伴有短暂的网络功能障碍。
IF 3.6 4区 医学
Cellular and Molecular Neurobiology Pub Date : 2025-01-02 DOI: 10.1007/s10571-024-01516-y
Atiyeh Mohammadshirazi, Graciela L Mazzone, Benjamín A Zylberberg, Giuliano Taccola
{"title":"A Focal Traumatic Injury to the Neonatal Rodent Spinal Cord Causes an Immediate and Massive Spreading Depolarization Sustained by Chloride Ions, with Transient Network Dysfunction.","authors":"Atiyeh Mohammadshirazi, Graciela L Mazzone, Benjamín A Zylberberg, Giuliano Taccola","doi":"10.1007/s10571-024-01516-y","DOIUrl":"10.1007/s10571-024-01516-y","url":null,"abstract":"<p><p>In clinics, physical injuries to the spinal cord cause a temporary motor areflexia below lesion, known as spinal shock. This topic is still underexplored due to the lack of preclinical spinal cord injury (SCI) models that do not use anesthesia, which would affect spinal excitability. Our innovative design considered a custom-made micro impactor that provides localized and calibrated strikes to the ventral surface of the thoracic spinal cord of the entire CNS isolated from neonatal rats. Before and after injury, multiple ventral root (VR) recordings continuously traced respiratory rhythm, baseline spontaneous activities, and electrically induced reflex responses. As early as 200 ms after the lowering of the impactor, an immediate transient depolarization spread from the injury site to the whole spinal cord with distinct segmental velocities. Stronger strikes induced higher potentials causing, close by the site of injury, a transient drop in spinal cord oxygenation (SCO<sub>2</sub>) and a massive cell death with a complete functional disconnection of input along the cord. Below the impact site, expiratory rhythm and spontaneous lumbar activity were suppressed. On lumbar VRs, reflex responses transiently halted but later recovered to control values, while electrically induced fictive locomotion remained perturbed. Moreover, low-ion modified Krebs solutions differently influenced impact-induced depolarizations, the magnitude of which amplified in low Cl<sup>-</sup>. Overall, our novel ex vivo platform traces the immediate functional consequences of impacts to the spinal cord during development. This basic study provides insights on the SCI pathophysiology, unveiling an immediate chloride dysregulation.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"10"},"PeriodicalIF":3.6,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11695467/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142913268","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
Differences in Blood and Cerebrospinal Fluid Between Parkinson's Disease and Related Diseases. 帕金森病及相关疾病患者血液和脑脊液的差异
IF 3.6 4区 医学
Cellular and Molecular Neurobiology Pub Date : 2024-12-27 DOI: 10.1007/s10571-024-01523-z
Jie Ma, Zhijian Tang, Yaqi Wu, Jun Zhang, Zitao Wu, Lulu Huang, Shengwen Liu, Yu Wang
{"title":"Differences in Blood and Cerebrospinal Fluid Between Parkinson's Disease and Related Diseases.","authors":"Jie Ma, Zhijian Tang, Yaqi Wu, Jun Zhang, Zitao Wu, Lulu Huang, Shengwen Liu, Yu Wang","doi":"10.1007/s10571-024-01523-z","DOIUrl":"10.1007/s10571-024-01523-z","url":null,"abstract":"<p><p>It is difficult to distinguish Parkinson's disease (PD) in the early stage from those of various disorders including atypical Parkinson's syndrome (APS), vascular parkinsonism (VP), and even essential tremor (ET), because of the overlap of symptoms. Other, more challenging problems will arise when Parkinson's disease develops into Parkinson's disease dementia (PDD) in the middle and late stages. At this time, the differential diagnosis of PDD and DLB becomes thorny. These complicate the diagnostic process for PD, which traditionally heavily relies on symptomatic assessment and treatment response. Recent advances have identified several biomarkers in the blood and cerebrospinal fluid (CSF), including α-synuclein, lysosomal enzymes, fatty acid-binding proteins, and neurofilament light chain, whose concentration differs in PD and the related diseases. However, not all these molecules can effectively discriminate PD from related disorders. This review advocates for a paradigm shift toward biomarker-based diagnosis to effectively distinguish between PD and similar conditions. These biomarkers may reflect the diversity that exist among different diseases and provide an effective way to accurately understand their mechanisms. This review focused on blood and CSF biomarkers of PD that may have differential diagnostic value and the related molecular measurement methods with high diagnostic performance due to emerging technologies.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"9"},"PeriodicalIF":3.6,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11680620/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142892426","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
Molecular Signaling Pathways of Quercetin in Alzheimer's Disease: A Promising Arena. 槲皮素在阿尔茨海默病中的分子信号通路:一个有前景的领域。
IF 3.6 4区 医学
Cellular and Molecular Neurobiology Pub Date : 2024-12-24 DOI: 10.1007/s10571-024-01526-w
Mansour A Alsaleem, Hayder M Al-Kuraishy, Ali I Al-Gareeb, Ali K Albuhadily, Mohammed Alrouji, Asmaa S A Yassen, Athanasios Alexiou, Marios Papadakis, Gaber El-Saber Batiha
{"title":"Molecular Signaling Pathways of Quercetin in Alzheimer's Disease: A Promising Arena.","authors":"Mansour A Alsaleem, Hayder M Al-Kuraishy, Ali I Al-Gareeb, Ali K Albuhadily, Mohammed Alrouji, Asmaa S A Yassen, Athanasios Alexiou, Marios Papadakis, Gaber El-Saber Batiha","doi":"10.1007/s10571-024-01526-w","DOIUrl":"10.1007/s10571-024-01526-w","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a neurodegenerative disease characterized by cognitive impairment and memory deficit. Even with extensive research and studies, presently, there is no effective treatment for the management of AD. Besides, most of drugs used in the treatment of AD did not avert the AD neuropathology, and the disease still in a progressive status. For example, acetyl cholinesterase inhibitors are associated with many adverse effects, such as insomnia and nightmares. As well, acetylcholinesterase inhibitors augment cholinergic neurotransmission leading to the development of adverse effects related to high acetylcholine level, such as salivation, rhinorrhea, vomiting, loss of appetite, and seizure. Furthermore, tacrine has poor bioavailability and causes hepatotoxicity. These commonly used drugs do not manage the original causes of AD. For those reasons, natural products were repurposed for the treatment of AD and neurodegenerative diseases. It has been shown that phytochemicals produce neuroprotective effects against the development and progression of neurodegenerative diseases by different mechanisms, including antioxidant and anti-inflammatory effects. Quercetin (QCN) has been reported to exert an effective neuroprotective effect against AD and other neurodegenerative diseases by lessening oxidative stress. In this review, electronic databases such as PubMed, Scopus, and Web of Science were searched for possible relevant studies and article linking the effect of QCN on AD. Findings from this review highlighted that many studies highlighted different mechanistic signaling pathways regarding the neuroprotective effect of QCN in AD. Nevertheless, the precise molecular mechanism of QCN in AD was not completely clarified. Consequently, this review aims to discuss the molecular mechanism of QCN in AD.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"8"},"PeriodicalIF":3.6,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11668837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142884975","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
Glucocorticoid-Dependent Retinal Degeneration and Vision Impairment in Mice Susceptible to Prenatal Stress-Induced Behavioral Abnormalities. 糖皮质激素依赖性视网膜变性和视力障碍小鼠易受产前应激诱导的行为异常。
IF 3.6 4区 医学
Cellular and Molecular Neurobiology Pub Date : 2024-12-23 DOI: 10.1007/s10571-024-01525-x
Min-Ok Ryu, Ji-Youl Jung, Han Na Suh, Chung-Young Lee, Myung-Chul Kim, Ji Young Oh, Woo-Jin Song, Changhwan Ahn, Yeseul Yang, Gee Euhn Choi
{"title":"Glucocorticoid-Dependent Retinal Degeneration and Vision Impairment in Mice Susceptible to Prenatal Stress-Induced Behavioral Abnormalities.","authors":"Min-Ok Ryu, Ji-Youl Jung, Han Na Suh, Chung-Young Lee, Myung-Chul Kim, Ji Young Oh, Woo-Jin Song, Changhwan Ahn, Yeseul Yang, Gee Euhn Choi","doi":"10.1007/s10571-024-01525-x","DOIUrl":"10.1007/s10571-024-01525-x","url":null,"abstract":"<p><p>Chronic exposure to prenatal stress can impair neurogenesis and lead to irreversible cognitive and neuropsychiatric abnormalities in offspring. The retina is part of the nervous system; however, the impacts of prenatal stress on retinal neurogenesis and visual function remain unclear. This study examined how elevated prenatal glucocorticoid levels differentially affect retinal development in the offspring of pregnant mice exposed to chronic unpredictable mild stress (CUMS). Offspring were classified into control, stress-resilient, and stress-susceptible groups based on behavioral tests assessing spatial memory and depression-like behaviors. The stress-susceptible group exhibited significantly altered synaptogenesis, reduced ganglion cell development, decreased retinal thickness, and visiual impairment. These mice also showed a pervasive transformation of retinal astrocytes into a proinflammatory A1-like reactive state, evidenced by increased GFAP and decreased STAT3 expression levels. This astrocyte phenotype shift coincided with disruptions in neurogenesis and synaptic formation. Furthermore, prenatal exposure to exogenous corticosterone confirmed that the effects of prenatal stress are mediated by glucocorticoid-induced retinal neurodegeneration. Our findings suggest that elevated prenatal glucocorticoid levels trigger a series of neurodevelopmental disturbances leading to retinal neurodegeneration and vision impairment. This research highlights the impact of prenatal stress on retinal development and visual health, suggesting new avenues for understanding and potentially mitigating the negative effects of early-life stress on neurodevelopment.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"7"},"PeriodicalIF":3.6,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11666777/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876286","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
Application of Circulating Tumor DNA in the Auxiliary Diagnosis and Prognosis Prediction of Glioma. 循环肿瘤DNA在胶质瘤辅助诊断及预后预测中的应用。
IF 3.6 4区 医学
Cellular and Molecular Neurobiology Pub Date : 2024-12-18 DOI: 10.1007/s10571-024-01515-z
Ying Lu, Zhouyu Wang, Danmeng Zhang, Ningning Luo, Hui Yang, Dongsheng Chen, Haixin Huang
{"title":"Application of Circulating Tumor DNA in the Auxiliary Diagnosis and Prognosis Prediction of Glioma.","authors":"Ying Lu, Zhouyu Wang, Danmeng Zhang, Ningning Luo, Hui Yang, Dongsheng Chen, Haixin Huang","doi":"10.1007/s10571-024-01515-z","DOIUrl":"10.1007/s10571-024-01515-z","url":null,"abstract":"<p><p>Glioma is the most common primary malignant brain tumor. Despite significant advances in the past decade in understanding the molecular pathogenesis of this tumor and exploring therapeutic strategies, the prognosis of patients with glioma remains poor. Accurate diagnosis of glioma is very important for the treatment and prognosis. Although the gold-standard method for the diagnosis and prognosis prediction of patients with glioma is tissue biopsy, it still has many limitations. Liquid biopsy can provide information on the auxiliary diagnosis and prognosis of gliomas. In this review, we summarized the application of cell-free DNA (cfDNA) and circulating tumor DNA (ctDNA) in the auxiliary diagnosis and prognosis of glioma. The common methods used to detect ctDNA in gliomas using samples including blood and cerebrospinal fluid (CSF) and the detection techniques for ctDNA, including droplet digital PCR (ddPCR) and next-generation sequencing (NGS), were discussed. Detection of ctDNA from plasma of patients with brain tumors remains challenging because of the blood-brain barrier (BBB). CSF has been proposed as a medium for ctDNA analysis in brain tumors, and mutation detection using plasma ctDNA was less sensitive than CSF ctDNA sequencing. Moreover, ongoing relevant clinical studies were summarized. Finally, we discussed the challenges, and future directions for the studies on ctDNA in glioma.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"6"},"PeriodicalIF":3.6,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11655607/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846176","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
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