Neuroscience Research最新文献_第10页

Dynamic neuronal instability generates synaptic plasticity and behavior: Insights from Drosophila sleep 动态神经元不稳定性产生突触可塑性和行为果蝇睡眠的启示

IF 2.9 4区医学

Neuroscience Research Pub Date : 2024-01-01 DOI: 10.1016/j.neures.2023.06.009

Masashi Tabuchi

{"title":"Dynamic neuronal instability generates synaptic plasticity and behavior: Insights from Drosophila sleep","authors":"Masashi Tabuchi","doi":"10.1016/j.neures.2023.06.009","DOIUrl":"10.1016/j.neures.2023.06.009","url":null,"abstract":"<div><p>How do neurons encode the information that underlies cognition, internal states, and behavior? This review focuses on the neural circuit mechanisms underlying sleep in <em>Drosophila</em> and, to illustrate the power of addressing neural coding in this system, highlights a specific circuit mediating the circadian regulation of sleep quality. This circuit exhibits circadian cycling of sleep quality, which depends solely on the pattern (not the rate) of spiking. During the night, the stability of spike waveforms enhances the reliability of spike timing in these neurons to promote sleep quality. During the day, instability of the spike waveforms leads to uncertainty of spike timing, which remarkably produces synaptic plasticity to induce arousal. Investigation of the molecular and biophysical basis of these changes was greatly facilitated by its study in <em>Drosophila</em>, revealing direct connections between genes, molecules, spike biophysical properties, neural codes, synaptic plasticity, and behavior. Furthermore, because these patterns of neural activity change with aging, this model system holds promise for understanding the interplay between the circadian clock, aging, and sleep quality. It is proposed here that neurophysiological investigations of the <em>Drosophila</em> brain present an exceptional opportunity to tackle some of the most challenging questions related to neural coding.</p></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"198 ","pages":"Pages 1-7"},"PeriodicalIF":2.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0168010223001335/pdfft?md5=54927ae8aa6dee1edac124c9aea54375&pid=1-s2.0-S0168010223001335-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9736442","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

Prolonged stress-induced depression-like behaviors in aged rats are mediated by endoplasmic reticulum stress and apoptosis in the hippocampus 老年大鼠长期应激诱发的抑郁样行为是由海马内质网应激和细胞凋亡介导的

IF 2.9 4区医学

Neuroscience Research Pub Date : 2024-01-01 DOI: 10.1016/j.neures.2023.06.011

Arshad Ghaffari-Nasab , Gonja Javani , Hadi Yousefi , Rahim Sharafkhani , Sajjad Taghizadeh

{"title":"Prolonged stress-induced depression-like behaviors in aged rats are mediated by endoplasmic reticulum stress and apoptosis in the hippocampus","authors":"Arshad Ghaffari-Nasab , Gonja Javani , Hadi Yousefi , Rahim Sharafkhani , Sajjad Taghizadeh","doi":"10.1016/j.neures.2023.06.011","DOIUrl":"10.1016/j.neures.2023.06.011","url":null,"abstract":"<div><p>Structural and functional recovery from stress-induced depression is impaired in the context of aging brain. Since investigating the molecular substrates that facilitate behavioral recovery may have important implications for understanding brain plasticity and resilience of individuals, we studied depressive-like behaviors in young and aged rats 6 weeks after chronic stress exposure as a recovery period and examined the levels of TNF-α and IL-6 inflammatory cytokines, NADH oxidase activity, NADPH oxidase, endoplasmic reticulum (ER) stress markers, and apoptosis in the hippocampus. Young (3 months old) and aged (22 months old) male Wistar rats were divided into four groups; young control (Young), depression model of young rats that received chronic stress procedure followed by a 6-week recovery period (Young+S), aged control (Aged), and depression model of aged rats that received chronic stress procedure followed by a 6-week recovery period (Aged+S). After the recovery period, aged but not young rats showed depression-like behaviors, evaluated by the sucrose preference test (SPT) and forced swimming test (FST), coincided with the altered levels of TNF-α, IL-6, NADH oxidase activity, NADPH oxidase, GRP78, CHOP, and cleaved caspase-12 in the hippocampus of these animals. These data suggested that oxidative and ER stress-induced apoptosis in the aging hippocampus may affect the recovery-related outcomes after the stress paradigm.</p></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"198 ","pages":"Pages 39-46"},"PeriodicalIF":2.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0168010223001359/pdfft?md5=cc6805fa058de269d8496ad46d94b363&pid=1-s2.0-S0168010223001359-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10225456","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: 1

Quantifying acute changes in neurometabolism following blast-induced traumatic brain injury 量化爆炸诱发创伤性脑损伤后神经代谢的急性变化

IF 2.9 4区医学

Neuroscience Research Pub Date : 2024-01-01 DOI: 10.1016/j.neures.2023.06.008

Carly Norris , Justin Weatherbee , Susan F. Murphy , Pamela J. VandeVord

{"title":"Quantifying acute changes in neurometabolism following blast-induced traumatic brain injury","authors":"Carly Norris , Justin Weatherbee , Susan F. Murphy , Pamela J. VandeVord","doi":"10.1016/j.neures.2023.06.008","DOIUrl":"10.1016/j.neures.2023.06.008","url":null,"abstract":"<div><p>Brain health is largely dependent on the metabolic regulation of amino acids. Brain injuries, diseases, and disorders can be detected through alterations in free amino acid (FAA) concentrations; and thus, mapping the changes has high diagnostic potential. Common methods focus on optimizing neurotransmitter quantification; however, recent focus has expanded to investigate the roles of molecular precursors in brain metabolism. An isocratic method using high performance liquid chromatography with electrochemical cell detection was developed to quantify a wide range of molecular precursors and neurotransmitters: alanine, arginine, aspartate, serine, taurine, threonine, tyrosine, glycine, glutamate, glutamine, and γ-Aminobutyric acid (GABA) following traumatic brain injury. First, baseline concentrations were determined in the serum, cerebrospinal fluid, hippocampus, cortex, and cerebellum of naïve male Sprague Dawley rats. A subsequent study was performed investigating acute changes in FAA concentrations following blast-induced traumatic brain injury (bTBI). Molecular precursor associated FAAs decreased in concentration at 4 h after injury in both the cortex and hippocampus while those serving as neurotransmitters remained unchanged. In particular, the influence of oxidative stress on the observed changes within alanine and arginine pathways following bTBI should be further investigated to elucidate the full therapeutic potential of these molecular precursors at acute time points.</p></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"198 ","pages":"Pages 47-56"},"PeriodicalIF":2.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S016801022300130X/pdfft?md5=e691a08a599f008a13dcbb01bedfa88e&pid=1-s2.0-S016801022300130X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9814276","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

The therapeutic role of SSEA3(+) human umbilical cord blood mononuclear cells in ischemic stroke model SSEA3（+）人脐带血单核细胞在缺血性中风模型中的治疗作用。

IF 2.9 4区医学

Neuroscience Research Pub Date : 2023-12-26 DOI: 10.1016/j.neures.2023.12.006

Dongjie Xiao , Fang Li , Kun Zhang , Guojun Liu , Yunshan Wang , Hua Liu

{"title":"The therapeutic role of SSEA3(+) human umbilical cord blood mononuclear cells in ischemic stroke model","authors":"Dongjie Xiao , Fang Li , Kun Zhang , Guojun Liu , Yunshan Wang , Hua Liu","doi":"10.1016/j.neures.2023.12.006","DOIUrl":"10.1016/j.neures.2023.12.006","url":null,"abstract":"<div><p>Numerous evidences showed that human umbilical cord blood (UCB) mononuclear cells were a promising approach for the therapy of ischemic stroke(IS). The effect of stage-specific embryonic antigen 3 (SSEA3）positive subpopulation in UCB was not investigated in IS. In this study, we isolated SSEA3 positive cells from healthy UCB mononuclear cells, which comprised about 7.01% of the total UCB-mononuclear cells. Flow cytometry analysis revealed that SSEA3(+)UCB cells were almost positive for CD44 and CD45, and negative for CD73, CD90 and CD105. The expression of Oct3/4 in SSEA3(+)UCB cells were higher than that in UCB. SSEA3(+)UCB cells sorted by magnetic cell sorting were intravenously injected into the middle cerebral arterial occlusion(MCAO) rat model. Neurological score showed that SSEA3(+)UCB transplantation group exhibited significant improvements in the functional outcome of MCAO rats than UCB transplantation group. Nissl staining and microtubule association protein-2(MAP2) immunofluorescence staining showed that the SSEA3(+)UCB transplantation group decreased neuronal loss. SSEA3(+)UCB transplantation group reduced neuronal apoptosis, inhibited caspase3 expression, and decreased tumor necrosis factor α(TNF-α). These results indicate that SSEA3 positive cells are a novel subpopulation of UCB cells, which exhibit great potential for the treatment of ischemic stroke.</p></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"203 ","pages":"Pages 42-50"},"PeriodicalIF":2.9,"publicationDate":"2023-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0168010223002237/pdfft?md5=ab003d840112aff6aceb8ec050dad612&pid=1-s2.0-S0168010223002237-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139058561","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

Two common issues in synchronized multimodal recordings with EEG: Jitter and latency 脑电图同步多模态记录的两个常见问题：抖动和延迟

IF 2.9 4区医学

Neuroscience Research Pub Date : 2023-12-22 DOI: 10.1016/j.neures.2023.12.003

Seitaro Iwama , Mitsuaki Takemi , Ryo Eguchi , Ryotaro Hirose , Masumi Morishige , Junichi Ushiba

{"title":"Two common issues in synchronized multimodal recordings with EEG: Jitter and latency","authors":"Seitaro Iwama , Mitsuaki Takemi , Ryo Eguchi , Ryotaro Hirose , Masumi Morishige , Junichi Ushiba","doi":"10.1016/j.neures.2023.12.003","DOIUrl":"10.1016/j.neures.2023.12.003","url":null,"abstract":"<div><p>Multimodal recording using electroencephalogram (EEG) and other biological signals (e.g., muscle activities, eye movement, pupil diameters, or body kinematics data) is ubiquitous in human neuroscience research. However, the precise time alignment of multiple data from heterogeneous sources (i.e., devices) is often arduous due to variable recording parameters of commercially available research devices and complex experimental setups. In this review, we introduced the versatility of a Lab Streaming Layer (LSL)-based application that can overcome two common issues in measuring multimodal data: jitter and latency. We discussed the issues of jitter and latency in multimodal recordings and the benefits of time-synchronization when recording with multiple devices. In addition, a computer simulation was performed to highlight how the millisecond-order jitter readily affects the signal-to-noise ratio of the electrophysiological outcome. Together, we argue that the LSL-based system can be used for research requiring precise time-alignment of datasets. Studies that detect stimulus-induced transient neural responses or test hypotheses regarding temporal relationships of different functional aspects with multimodal data would benefit most from LSL-based systems.</p></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"203 ","pages":"Pages 1-7"},"PeriodicalIF":2.9,"publicationDate":"2023-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0168010223002201/pdfft?md5=1a551f0703704d6ad1d5d6b046a4638c&pid=1-s2.0-S0168010223002201-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138985941","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

Nicotinic acetylcholine receptor activation induces BACE1 transcription via the phosphorylation and stabilization of nuclear SP1 烟碱乙酰胆碱受体激活通过核 SP1 的磷酸化和稳定诱导 BACE1 转录

IF 2.9 4区医学

Neuroscience Research Pub Date : 2023-12-16 DOI: 10.1016/j.neures.2023.12.002

Masaki Nakano , Tomohiro Tsuchida , Yachiyo Mitsuishi , Masaki Nishimura

{"title":"Nicotinic acetylcholine receptor activation induces BACE1 transcription via the phosphorylation and stabilization of nuclear SP1","authors":"Masaki Nakano , Tomohiro Tsuchida , Yachiyo Mitsuishi , Masaki Nishimura","doi":"10.1016/j.neures.2023.12.002","DOIUrl":"10.1016/j.neures.2023.12.002","url":null,"abstract":"<div><p>Epidemiological studies have shown that cigarette smoking increases the risk of Alzheimer disease. However, inconsistent results have been reported regarding the effects of smoking or nicotine on brain amyloid β (Aβ) deposition. In this study, we found that stimulation of the nicotinic acetylcholine receptor (nAChR) increased Aβ production in mouse brains and cultured neuronal cells. nAChR activation triggered the MEK/ERK pathway, which then phosphorylated and stabilized nuclear SP1. Upregulated SP1 acted on two recognition motifs in the BACE1 gene to induce its transcription, resulting in enhanced Aβ production. Mouse brain microdialysis revealed that nAChR agonists increased Aβ levels in the interstitial fluid of the cerebral cortex but caused no delay of Aβ clearance. In vitro assays indicated that nicotine inhibited Aβ aggregation. We also found that nicotine modified the immunoreactivity of anti-Aβ antibodies, possibly through competitive inhibition and Aβ conformation changes. Using anti-Aβ antibody that was carefully selected to avoid these effects, we found that chronic nicotine treatment in Aβ precursor protein knockin mice increased the Aβ content but did not visibly change the aggregated Aβ deposition in the brain. Thus, nicotine influences brain Aβ deposition in the opposite direction, thereby increasing Aβ production and inhibiting Aβ aggregation.</p></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"203 ","pages":"Pages 28-41"},"PeriodicalIF":2.9,"publicationDate":"2023-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0168010223002195/pdfft?md5=2058e3589e984b0ea161e9520c0c24b1&pid=1-s2.0-S0168010223002195-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138684008","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

Unveiling the regulatory of miR-101-3p on ZNF746 in a Parkinson's disease cell model: Implications for therapeutic targeting 揭示帕金森病细胞模型中 miR-101-3p 对 ZNF746 的调控作用：治疗靶点的意义

IF 2.9 4区医学

Neuroscience Research Pub Date : 2023-12-14 DOI: 10.1016/j.neures.2023.12.001

Maryam Mahmoudian Esfahani , Maryam Mostashfi , Shiva Vaheb Hosseinabadi , Motahare-Sadat Hashemi , Maryam Peymani , Dina Zohrabi , Seyed Abdolhamid Angaji , Mohammad Hossein Nasr-Esfahani , Kamran Ghaedi

{"title":"Unveiling the regulatory of miR-101-3p on ZNF746 in a Parkinson's disease cell model: Implications for therapeutic targeting","authors":"Maryam Mahmoudian Esfahani , Maryam Mostashfi , Shiva Vaheb Hosseinabadi , Motahare-Sadat Hashemi , Maryam Peymani , Dina Zohrabi , Seyed Abdolhamid Angaji , Mohammad Hossein Nasr-Esfahani , Kamran Ghaedi","doi":"10.1016/j.neures.2023.12.001","DOIUrl":"10.1016/j.neures.2023.12.001","url":null,"abstract":"<div><p>In this study, we explored the regulatory role of microRNA miR-101-3p on the zinc finger protein 746 (ZNF746), also known as PARIS, which is implicated in both sporadic and familial forms of Parkinson's disease. In a Parkinson's disease cell model, utilizing SH-SY5Y cells treated with 1-methyl-4-phenylpyridine (MPP+), we observed that miR-101–3p was downregulated, while ZNF746 was upregulated. To investigate the direct impact of miR-101-3p on ZNF746, our team conducted overexpression experiments, successfully reversing ZNF746's expression at both the mRNA and protein levels, as confirmed through quantitative PCR and western blotting. We also performed luciferase assays, providing compelling evidence that ZNF746 is a direct target of miR-101-3p. Additionally, we noted that miR-101-3p overexpression resulted in increased expression of PGC1α, a gene targeted by ZNF746. Functionally, we assessed the implications of miR-101-3p overexpression through MTS assays and flow cytometry, revealing significant promotion of cell viability, inhibition of ROS production, and reduced apoptosis in the Parkinson's disease cell model. In conclusion, this study highlights the role of miR-101-3p in regulating ZNF746 expression and suggests its potential as a therapeutic target for Parkinson's disease. These findings provide valuable molecular insights that could pave the way for innovative treatment strategies in combating this debilitating neurodegenerative disorder.</p></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"203 ","pages":"Pages 18-27"},"PeriodicalIF":2.9,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S016801022300216X/pdfft?md5=1f81dcc751f3c553fd4d1c78d722336f&pid=1-s2.0-S016801022300216X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138683737","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

Mechanisms of axonal degeneration and regeneration of the nervous system 神经系统轴索变性和再生的机制。

IF 2.9 4区医学

Neuroscience Research Pub Date : 2023-12-01 DOI: 10.1016/j.neures.2023.10.003

Miki Otsuki, Marco Terenzio

引用次数: 0

NMN: The NAD precursor at the intersection between axon degeneration and anti-ageing therapies NMN：轴突变性与抗衰老疗法交汇处的 NAD 前体

IF 2.9 4区医学

Neuroscience Research Pub Date : 2023-12-01 DOI: 10.1016/j.neures.2023.01.004

Andrea Loreto, Christina Antoniou, Elisa Merlini, Jonathan Gilley, Michael P. Coleman

{"title":"NMN: The NAD precursor at the intersection between axon degeneration and anti-ageing therapies","authors":"Andrea Loreto, Christina Antoniou, Elisa Merlini, Jonathan Gilley, Michael P. Coleman","doi":"10.1016/j.neures.2023.01.004","DOIUrl":"10.1016/j.neures.2023.01.004","url":null,"abstract":"<div><p>The past 20 years of research on axon degeneration has revealed fine details on how NAD biology controls axonal survival. Extensive data demonstrate that the NAD precursor NMN binds to and activates the pro-degenerative enzyme SARM1, so a failure to convert sufficient NMN into NAD leads to toxic NMN accumulation and axon degeneration. This involvement of NMN brings the axon degeneration field to an unexpected overlap with research into ageing and extending healthy lifespan. A decline in NAD levels throughout life, at least in some tissues, is believed to contribute to age-related functional decay and boosting NAD production with supplementation of NMN or other NAD precursors has gained attention as a potential anti-ageing therapy. Recent years have witnessed an influx of NMN-based products and related molecules on the market, sold as food supplements, with many people taking these supplements daily. While several clinical trials are ongoing to check the safety profiles and efficacy of NAD precursors, sufficient data to back their therapeutic use are still lacking. Here, we discuss NMN supplementation, SARM1 and anti-ageing strategies, with an important question in mind: considering that NMN accumulation can lead to axon degeneration, how is this compatible with its beneficial effect in ageing and are there circumstances in which NMN supplementation could become harmful?</p></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"197 ","pages":"Pages 18-24"},"PeriodicalIF":2.9,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0168010223000044/pdfft?md5=7fc5548b92bc540926f27e6d94a006a1&pid=1-s2.0-S0168010223000044-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9109645","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: 5

Number of kinesins engaged in axonal cargo transport: A novel biomarker for neurological disorders 参与轴突货物运输的驱动蛋白数量：一种新的神经疾病生物标志物。

IF 2.9 4区医学

Neuroscience Research Pub Date : 2023-12-01 DOI: 10.1016/j.neures.2023.09.004

Kumiko Hayashi , Kazuo Sasaki

{"title":"Number of kinesins engaged in axonal cargo transport: A novel biomarker for neurological disorders","authors":"Kumiko Hayashi , Kazuo Sasaki","doi":"10.1016/j.neures.2023.09.004","DOIUrl":"10.1016/j.neures.2023.09.004","url":null,"abstract":"<div><p>Kinesin motor proteins play crucial roles in anterograde transport of cargo vesicles in neurons, moving them along axons from the cell body towards the synaptic region. Not only the transport force and velocity of single motor protein, but also the number of kinesin molecules involved in transporting a specific cargo, is pivotal for synapse formation. This collective transport by multiple kinesins ensures stable and efficient cargo transport in neurons. Abnormal increases or decreases in the number of engaged kinesin molecules per cargo could potentially act as biomarkers for neurodegenerative diseases such as Alzheimer's, Parkinson's, amyotrophic lateral sclerosis (ALS), spastic paraplegia, polydactyly syndrome, and virus transport disorders. We review here a model constructed using physical measurements to quantify the number of kinesin molecules associated with their cargo, which could shed light on the molecular mechanisms of neurodegenerative diseases related to axonal transport.</p></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"197 ","pages":"Pages 25-30"},"PeriodicalIF":2.9,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0168010223001694/pdfft?md5=df6317651a4faa6565849394fc347818&pid=1-s2.0-S0168010223001694-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41147636","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: 1