Molecular and Cellular Neuroscience最新文献

{"title":"Interrogating mediators of single-cell transcriptional changes in the acute damaged cerebral cortex: Insights into endothelial-astrocyte interactions","authors":"Caroline de Jager ,&nbsp;Eman Soliman ,&nbsp;Michelle H. Theus","doi":"10.1016/j.mcn.2025.104003","DOIUrl":"10.1016/j.mcn.2025.104003","url":null,"abstract":"<div><div>Traumatic brain injury (TBI) induces complex cellular and molecular changes, challenging recovery and therapeutic development. Although molecular pathways have been implicated in TBI pathology, the cellular specificity of these mechanisms remains underexplored. Here, we investigate the role of endothelial cell (EC) EphA4, a receptor tyrosine kinase receptor involved in axonal guidance, in modulating cell-specific transcriptomic changes within the damaged cerebral cortex. Utilizing single-cell RNA sequencing (scRNA-seq) in an experimental TBI model, we mapped transcriptional changes across various cell types, with a focus on astrocytes and ECs. Our analysis reveals that EC-specific knockout (KO) of EphA4 triggers significant alterations in astrocyte gene expression and shifts predominate subclusters. We identified six distinct astrocyte clusters (C0–C5) in the damaged cortex including as C0-<em>Mobp</em>/<em>Plp1</em>+; C1-<em>Slc1a3</em>/<em>Clu</em>+; C2-<em>Hbb-bs</em>/<em>Hba-a1</em>/<em>Ndrg2</em>+; <em>C3-GFAP</em>/<em>Lcn2+</em>; C4-<em>Gli3</em>/<em>Mertk+</em>, and C5-<em>Cox8a+</em>. We validate a new Sox9+ cluster expressing Mertk and Gas, which mediates efferocytosis to facilitate apoptotic cell clearance and anti-inflammatory responses. Transcriptomic and CellChat analyses of EC-KO cells highlights upregulation of neuroprotective pathways, including increased amyloid precursor protein (<em>APP</em>) and <em>Gas6</em>. Key pathways predicted to be modulated in astrocytes from EC-KO mice include oxidative phosphorylation and FOXO signaling, mitochondrial dysfunction and ephrin B signaling. Concurrently, metabolic and signaling pathways in endothelial cells—such as ceramide and sphingosine phosphate metabolism and NGF-stimulated transcription—indicate an adaptive response to a metabolically demanding post-injury hypoxic environment. These findings elucidate potential interplay between astrocytic and endothelial responses as well as transcriptional networks underlying cortical tissue damage.</div></div>","PeriodicalId":18739,"journal":{"name":"Molecular and Cellular Neuroscience","volume":"133 ","pages":"Article 104003"},"PeriodicalIF":2.6,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143639751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RBM15 relies on m6A modification to inhibit UBE2C, alleviating hippocampal neuronal injury by limiting microglial inflammation","authors":"Yuehong Wan,&nbsp;Qin Kang,&nbsp;Ji Zhang,&nbsp;Canru Yu,&nbsp;Susu Fang,&nbsp;Dongqin Zou,&nbsp;Wen Chai","doi":"10.1016/j.mcn.2025.103996","DOIUrl":"10.1016/j.mcn.2025.103996","url":null,"abstract":"<div><h3>Background</h3><div>Microglia are strongly implicated in the development and progression of epilepsy, yet their impact on pathology remains unclear. This study aimed to explore the effects of ubiquitin-conjugating enzyme 2C (UBE2C) m6A methylation on microglial activation and neuronal injury in epilepsy.</div></div><div><h3>Methods</h3><div>A mouse model of pilocarpine-induced status epilepticus was constructed, and an in vitro system of HT22 hippocampal neurons was induced with Mg²⁺-free medium and cocultured with BV2 cells. The secretion of TNF-α, IL-6 and iNOS from BV2 cells was measured via qRT–PCR and ELISA. CCK-8 and flow cytometry were performed to verify cell viability and apoptosis. RNA degradation, RIP and Me-RIP assays were performed.</div></div><div><h3>Results</h3><div>RBM15 levels were decreased, whereas UBE2C levels were increased in the hippocampi of epileptic mice. Silencing UBE2C or overexpressing RBM15 suppressed the release of inflammatory cytokines (TNF-α and IL-6) and the M1 microglia activation marker iNOS in Mg²⁺-free BV2 cells, thereby limiting damage to hippocampal injured neurons. Mechanistically, RBM15 bound to UBE2C mRNA and decreased its stability via m6A methylation. Additionally, RBM15 inhibited the inflammatory activation of BV2 and HT22 neuron injury by inhibiting UBE2C.</div></div><div><h3>Conclusion</h3><div>The increase in UBE2C m6A modification induced by RBM15 upregulation inhibits hippocampal neuron damage through the suppression of microglial inflammation, providing important clues and potential targets for novel therapeutics for epilepsy.</div></div>","PeriodicalId":18739,"journal":{"name":"Molecular and Cellular Neuroscience","volume":"133 ","pages":"Article 103996"},"PeriodicalIF":2.6,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"P2X7 receptor augments kainic acid-induced nitrosative stress by abrogating GS-HSP25-mediated iNOS inhibition and GSH synthesis in the mouse hippocampus","authors":"Ji-Eun Kim,&nbsp;Duk-Shin Lee,&nbsp;Su Hyeon Wang,&nbsp;Tae-Cheon Kang","doi":"10.1016/j.mcn.2025.103995","DOIUrl":"10.1016/j.mcn.2025.103995","url":null,"abstract":"<div><div>Glutathione (GSH) and heat shock protein 25 (HSP25) reciprocally regulate each other, which maintain redox homeostasis. Since P2X7 receptor (P2X7R) regulates GSH biosynthesis and HSP25 induction, the present study was conducted to explore the role of P2X7R in the reciprocal regulation between HSP25 and GSH in response to kainic acid (KA)-induced nitrosative stress and the related signal pathways, which are largely unknown. The present data demonstrate that <em>P2X7R</em> deletion attenuated KA-induced reductions in total GSH level and nuclear factor-erythroid 2-related factor 2 (Nrf2) intensity/nuclear translocation in astrocytes. <em>P2X7R</em> ablation increased Nrf2 intensity/nuclear translocation in microglia following KA treatment. <em>P2X7R</em> deletion also ameliorated KA-induced inducible nitric oxide synthase (iNOS) and <em>S</em>-nitrosylated-cysteine (SNO-Cys) inductions in microglia and astrocytes. However, <em>P2X7R</em> ablation could not affect KA-induced nuclear Nrf2 translocation and SNO-Cys production in CA3 neurons. Furthermore, <em>P2X7R</em> ablation mitigated <em>S</em>-nitrosylations of glutamine synthase (GS) and alanine-serine-cysteine transporter 2 (ASCT2) induced by KA. <em>HSP25</em> knockdown increased GSH consumption, astroglial iNOS level and <em>S</em>-nitrosylations of GS and ASCT2, but decreased Nrf2 intensity/nuclear translocation in astrocytes of <em>P2X7R</em>^{<em>−/−</em>} mice following KA injection. These findings indicate that P2X7R facilitated iNOS upregulation by inhibiting HSP25 induction and nuclear Nrf2 translocation in astrocytes, which augmented nitrosative stress-mediated reduction in GSH biosynthesis in response to KA. Therefore, our data suggest that the targeting of P2X7R-Nrf2-iNOS-GS-HSP25 pathway may be required for the maintenance of GSH-mediated redox homeostasis against nitrosative stress, which would prevent the progression of undesirable consequences from seizures and neuroinflammation.</div></div>","PeriodicalId":18739,"journal":{"name":"Molecular and Cellular Neuroscience","volume":"133 ","pages":"Article 103995"},"PeriodicalIF":2.6,"publicationDate":"2025-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A microglial kinase ITK mediating neuroinflammation and behavioral deficits in traumatic brain injury","authors":"Ruqayya Afridi ,&nbsp;Anup Bhusal ,&nbsp;Seung Eun Lee ,&nbsp;Eun Mi Hwang ,&nbsp;Hoon Ryu ,&nbsp;Jong-Heon Kim ,&nbsp;Kyoungho Suk","doi":"10.1016/j.mcn.2025.103994","DOIUrl":"10.1016/j.mcn.2025.103994","url":null,"abstract":"<div><div>Microglia-mediated neuroinflammation has been implicated in the neuropathology of traumatic brain injuries (TBI). Recently, the expression of interleukin-2-inducible T-cell kinase (ITK) has been detected in brain microglia, regulating their inflammatory activities. However, the role of microglial ITK in TBI has not been investigated. In this study, we demonstrate that ITK expression and activation are upregulated in microglia following an injury caused by controlled cortical impact (CCI) – a mouse model of TBI. Pharmacological inhibition of ITK protein or knockdown of microglial ITK gene expression using adeno-associated virus mitigates neuroinflammation and improves neurological outcomes in the CCI model. Additionally, ITK mRNA expression was found to be increased in the brains of patients with chronic traumatic encephalopathy. An ITK inhibitor reduced the activation of inflammatory responses in both human and mouse microglia in vitro. Collectively, these results suggest that microglial ITK plays a pivotal role in neuroinflammation and mediating behavioral deficits following TBI. Thus, targeting the signaling pathway of microglial ITK may exert protective effects by alleviating neuroinflammation associated with TBI.</div></div>","PeriodicalId":18739,"journal":{"name":"Molecular and Cellular Neuroscience","volume":"132 ","pages":"Article 103994"},"PeriodicalIF":2.6,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143047155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial fission and fusion in neurodegenerative diseases:Ca2+ signalling","authors":"Xuan Liu ,&nbsp;Tianjiao Li ,&nbsp;Xinya Tu,&nbsp;Mengying Xu,&nbsp;Jianwu Wang","doi":"10.1016/j.mcn.2025.103992","DOIUrl":"10.1016/j.mcn.2025.103992","url":null,"abstract":"<div><div>Neurodegenerative diseases (NDs) are a group of disorders characterized by the progressive loss of neuronal structure and function. The pathogenesis is intricate and involves a network of interactions among multiple causes and systems. Mitochondria and Ca²⁺ signaling have long been considered to play important roles in the development of various NDs. Mitochondrial fission and fusion dynamics are important processes of mitochondrial quality control, ensuring the stability of mitochondrial structure and function. Mitochondrial fission and fusion imbalance and Ca²⁺ signaling disorders can aggravate the disease progression of NDs. In this review, we explore the relationship between mitochondrial dynamics and Ca²⁺ signaling in AD, PD, ALS, and HD, focusing on the roles of key regulatory proteins (Drp1, Fis1, Mfn1/2, and Opa1) and the association structures between mitochondria and the endoplasmic reticulum (MERCs/MAMs). We provide a detailed analysis of their involvement in the pathogenesis of these four NDs. By integrating these mechanisms, we aim to clarify their contributions to disease progression and offer insights into the development of therapeutic strategies that target mitochondrial dynamics and Ca²⁺ signaling. We also examine the progress in drug research targeting these pathways, highlighting their potential as therapeutic targets in the treatment of NDs.</div></div>","PeriodicalId":18739,"journal":{"name":"Molecular and Cellular Neuroscience","volume":"132 ","pages":"Article 103992"},"PeriodicalIF":2.6,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143040154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identifying potential genes driving ferroptosis in the substantia nigra and dopaminergic neurons in Parkinson's disease","authors":"Ardra Chakrabarti,&nbsp;Sonia Verma","doi":"10.1016/j.mcn.2025.103993","DOIUrl":"10.1016/j.mcn.2025.103993","url":null,"abstract":"<div><div>Parkinson's disease (PD) is a neurodegenerative disorder marked by dopaminergic (DA) neuron degeneration in the substantia nigra (SN). Conventional dopamine replacement therapies provide limited long-term efficacy and significant side effects. Emerging evidence suggests ferroptosis—a form of cell death driven by iron-dependent lipid peroxidation—contributes to PD pathology, though direct evidence linking dysregulation of ferroptosis-related genes in DA neuron loss in PD remains limited. This study explores the expression of ferroptosis-associated genes in the SN and DA neurons of PD patients, identifying potential therapeutic targets. We analyzed two independent RNA-seq datasets, GSE7621 and GSE8397 (GPL-96), from the GEO database to identify common differentially expressed ferroptosis-related genes in the SN of PD patients. We also conducted Gene Ontology and pathway enrichment analyses of these genes to explore the underlying mechanisms and constructed a protein-protein interaction network. The findings were further validated using an additional dataset, <span><span>GSE49036</span><svg><path></path></svg></span>. We further explored the dysregulation of these ferroptosis-related genes in DA neurons using RNA-seq data <span><span>GSE169755</span><svg><path></path></svg></span>, derived from DA neurons isolated from the SN of PD patients and controls. Lastly, the proposed hypothesis was experimentally validated in an in vitro PD model. This comprehensive multi-dataset analysis uncovers novel insights into the expression of ferroptosis-related genes in PD, suggesting potential biomarkers and therapeutic targets for mitigating DA neuron loss and PD progression.</div></div>","PeriodicalId":18739,"journal":{"name":"Molecular and Cellular Neuroscience","volume":"132 ","pages":"Article 103993"},"PeriodicalIF":2.6,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143029142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex-specific cognitive benefits and anti-inflammatory effects of coumestrol pretreatment in transient global cerebral ischemia","authors":"Cibele Canal Castro ,&nbsp;Adriana Vizuete ,&nbsp;Bruna Ferrary Deniz ,&nbsp;Angela Wyse ,&nbsp;Carlos Alexandre Netto","doi":"10.1016/j.mcn.2025.103991","DOIUrl":"10.1016/j.mcn.2025.103991","url":null,"abstract":"<div><div>Cerebral Global Ischemia (CGI) is a devastating neurological condition affecting millions globally each year, leading to significant inflammatory responses and long-term consequences, including delayed neuronal death and neurocognitive impairment. Following brain injury, resident microglial cells are activated, triggering pro-inflammatory cytokine expression and altering neuroimmune processes in a sex-dependent manner, particularly within the hippocampus. Coumestrol, a plant estrogen, is promoted as an alternative to post-menopausal hormone therapy due to its various mechanisms that enhance brain health, including its anti-inflammatory effects. This study aimed to investigate whether coumestrol pretreatment could attenuate the neuroinflammatory response following CGI by regulating pro-inflammatory pathways (GFAP, S100B, TNF-α, and IL-1β) and reversing CGI-induced memory loss.</div><div>Male and female rats underwent CGI for 10 min or a sham surgery and received an ICV infusion of 20 μg of coumestrol or vehicle 1 h before CGI induction. Our findings revealed intriguing sex-specific effects of coumestrol pretreatment on gliosis following CGI and reperfusion, suggesting modulation of glial responses after ischemic insults. Coumestrol pre-administration significantly reduced levels of pro-inflammatory cytokines TNF-α and IL-1β during both reperfusion periods in both sexes, thereby mitigating CGI-induced neuroinflammation. Moreover, coumestrol pretreatment effectively reduced stroke-induced cognitive impairment, alleviating ischemia-induced memory deficits in both male and female rats. These results demonstrate the coumestrol's ability to attenuate cognitive deficits induced by CGI and highlight its potential sex-specific effects on inflammatory pathways. This study suggests that coumestrol modulates the glial and microglial inflammatory response, offering a promising approach to mitigate memory deficits associated with cerebral global ischemia.</div></div>","PeriodicalId":18739,"journal":{"name":"Molecular and Cellular Neuroscience","volume":"132 ","pages":"Article 103991"},"PeriodicalIF":2.6,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143008449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microglia-like cells from patient monocytes demonstrate increased phagocytic activity in probable Alzheimer's disease","authors":"Ceren Perihan Gonul ,&nbsp;Cagla Kiser ,&nbsp;Emis Cansu Yaka ,&nbsp;Didem Oz ,&nbsp;Duygu Hunerli ,&nbsp;Deniz Yerlikaya ,&nbsp;Melis Olcum ,&nbsp;Pembe Keskinoglu ,&nbsp;Gorsev Yener ,&nbsp;Sermin Genc","doi":"10.1016/j.mcn.2024.103990","DOIUrl":"10.1016/j.mcn.2024.103990","url":null,"abstract":"<div><div>Alzheimer's disease (AD) is a neurodegenerative disorder that is characterized by the accumulation of amyloid plaques, phosphorylated tau tangles and microglia toxicity, resulting in neuronal death and cognitive decline. Since microglia are recognized as one of the key players in the disease, it is crucial to understand how microglia operate in disease conditions and incorporate them into models. The studies on human microglia functions are thought to reflect the post-symptomatic stage of the disease. Recently developed methods involve induced microglia-like cells (iMGs) generated from patients' blood monocytes or induced pluripotent stem cells (iPSCs) as an alternative to studying the microglia cells <em>in vitro</em>. In this research, we aimed to investigate the phenotype and inflammatory responses of iMGs from AD patients. Monocytes derived from blood using density gradient centrifugation were differentiated into iMGs using a cytokine cocktail, including granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-34 (IL-34). After differentiation, cells were assessed by morphological analysis and a microglia surface marker, TMEM119. We used stimulants, lipopolysaccharide (LPS) and beta-amyloid, to examine iMGs' functions. Results showed that iMGs derived from AD patients exhibited increased secretion of pro-inflammatory cytokines upon LPS stimulation. Furthermore, their phagocytic ability was also heightened in stimulated and unstimulated conditions, with cells derived from patients showing increased phagocytic activity compared to healthy controls. Overall, these findings suggest that iMGs derived from patients using the direct conversion method possess characteristics of human microglia, making them an easy and promising model for studying microglia function in AD.</div></div>","PeriodicalId":18739,"journal":{"name":"Molecular and Cellular Neuroscience","volume":"132 ","pages":"Article 103990"},"PeriodicalIF":2.6,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142896169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glutathione S-transferase: A keystone in Parkinson's disease pathogenesis and therapy","authors":"Pratyush Padhan ,&nbsp;Simran ,&nbsp;Neeraj Kumar ,&nbsp;Sonia Verma","doi":"10.1016/j.mcn.2024.103981","DOIUrl":"10.1016/j.mcn.2024.103981","url":null,"abstract":"<div><div>Parkinson's disease is a progressive neurodegenerative disorder that predominantly affects motor function due to the loss of dopaminergic neurons in the substantia nigra. It presents significant challenges, impacting millions worldwide with symptoms such as tremors, rigidity, bradykinesia, and postural instability, leading to decreased quality of life and increased morbidity. The pathogenesis of Parkinson's disease is multifaceted, involving complex interactions between genetic susceptibility, environmental factors, and aging, with oxidative stress playing a central role in neuronal degeneration. Glutathione S-Transferase enzymes are critical in the cellular defense mechanism against oxidative stress, catalysing the conjugation of the antioxidant glutathione to various toxic compounds, thereby facilitating their detoxification. Recent research underscores the importance of Glutathione S-Transferase in the pathophysiology of Parkinson's disease, revealing that genetic polymorphisms in Glutathione S-Transferase genes influence the risk and progression of the disease. These genetic variations can affect the enzymatic activity of Glutathione S-Transferase, thereby modulating an individual's capacity to detoxify reactive oxygen species and xenobiotics, which are implicated in Parkinson's disease neuropathological processes. Moreover, biochemical studies have elucidated the role of Glutathione S-Transferase in not only maintaining cellular redox balance but also in modulating various cellular signalling pathways, highlighting its neuroprotective potential. From a therapeutic perspective, targeting Glutathione S-Transferase pathways offers promising avenues for the development of novel treatments aimed at enhancing neuroprotection and mitigating disease progression. This review explores the evident and hypothesized roles of Glutathione S-Transferase in Parkinson's disease, providing a comprehensive overview of its importance and potential as a target for therapeutic intervention.</div></div>","PeriodicalId":18739,"journal":{"name":"Molecular and Cellular Neuroscience","volume":"132 ","pages":"Article 103981"},"PeriodicalIF":2.6,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142792063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microfluidics in neural extracellular vesicles characterization for early Alzheimer's disease diagnosis","authors":"Hossein Zare ,&nbsp;Michelle M. Kasdorf ,&nbsp;Amirala Bakhshian Nik","doi":"10.1016/j.mcn.2024.103982","DOIUrl":"10.1016/j.mcn.2024.103982","url":null,"abstract":"<div><div>Dementia is a general term for conditions impairing cognitive abilities including perception, reasoning, attention, judgment, memory, and daily brain function. Early diagnosis of Alzheimer's disease (AD), the most common form of dementia, using neural extracellular vesicles (nEVs) is the focus of the current study. These nEVs carry AD biomarkers including β-amyloid proteins and phosphorylated tau proteins. The novelty of this review lies in developing a microfluidic perspective by introducing the techniques using a microfluidic platform for early diagnosis of AD. A microfluidic device can detect small sample sizes with significantly low concentrations. These devices combine nEV isolation, enrichment, and detection, which makes them ideal candidates for early AD diagnosis.</div></div>","PeriodicalId":18739,"journal":{"name":"Molecular and Cellular Neuroscience","volume":"132 ","pages":"Article 103982"},"PeriodicalIF":2.6,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142780528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}