Relevant bibliographies by topics / Axonal transport

Academic literature on the topic 'Axonal transport'

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Published: 4 June 2021
Last updated: 30 July 2024

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Journal articles on the topic "Axonal transport"

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Miller, Kyle E., and Michael P. Sheetz. "Direct evidence for coherent low velocity axonal transport of mitochondria." Journal of Cell Biology 173, no. 3 (May 8, 2006): 373–81. http://dx.doi.org/10.1083/jcb.200510097.

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Axonal growth depends on axonal transport. We report the first global analysis of mitochondrial transport during axonal growth and pauses. In the proximal axon, we found that docked mitochondria attached to the cytoskeletal framework that were stationary relative to the substrate and fast axonal transport fully accounted for mitochondrial transport. In the distal axon, we found both fast mitochondrial transport and a coherent slow transport of the mitochondria docked to the axonal framework (low velocity transport [LVT]). LVT was distinct from previously described transport processes; it was coupled with stretching of the axonal framework and, surprisingly, was independent of growth cone advance. Fast mitochondrial transport decreased and LVT increased in a proximodistal gradient along the axon, but together they generated a constant mitochondrial flux. These findings suggest that the viscoelastic stretching/creep of axons caused by tension exerted by the growth cone, with or without advance, is seen as LVT that is followed by compensatory intercalated addition of new mitochondria by fast axonal transport.
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Spinner, Michael A., Katherine Pinter, Catherine M. Drerup, and Tory G. Herman. "A Conserved Role for Vezatin Proteins in Cargo-Specific Regulation of Retrograde Axonal Transport." Genetics 216, no. 2 (August 11, 2020): 431–45. http://dx.doi.org/10.1534/genetics.120.303499.

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Active transport of organelles within axons is critical for neuronal health. Retrograde axonal transport, in particular, relays neurotrophic signals received by axon terminals to the nucleus and circulates new material among en passant synapses. A single motor protein complex, cytoplasmic dynein, is responsible for nearly all retrograde transport within axons: its linkage to and transport of diverse cargos is achieved by cargo-specific regulators. Here, we identify Vezatin as a conserved regulator of retrograde axonal transport. Vertebrate Vezatin (Vezt) is required for the maturation and maintenance of cell-cell junctions and has not previously been implicated in axonal transport. However, a related fungal protein, VezA, has been shown to regulate retrograde transport of endosomes in hyphae. In a forward genetic screen, we identified a loss-of-function mutation in the Drosophila vezatin-like (vezl) gene. We here show that vezl loss prevents a subset of endosomes, including signaling endosomes containing activated BMP receptors, from initiating transport out of motor neuron terminal boutons. vezl loss also decreases the transport of endosomes and dense core vesicles, but not mitochondria, within axon shafts. We disrupted vezt in zebrafish and found that vezt loss specifically impairs the retrograde axonal transport of late endosomes, causing their accumulation in axon terminals. Our work establishes a conserved, cargo-specific role for Vezatin proteins in retrograde axonal transport.
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KUZNETSOV, A. V., A. A. AVRAMENKO, and D. G. BLINOV. "MODELING TRAFFIC JAMS IN SLOW AXONAL TRANSPORT." Journal of Mechanics in Medicine and Biology 10, no. 03 (September 2010): 445–65. http://dx.doi.org/10.1142/s0219519410003502.

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The purpose of this paper is to develop a model capable of simulating traffic jams in slow axonal transport. Slowing of slow axonal transport is an early sign of some neurodegenerative diseases. Axonal swellings observed near the end stage of such diseases may be an indication of traffic jams developing in axons that cause the slowing down of slow axonal transport. Traffic jams may result from misregulation of microtubule-associated proteins caused by an imbalance in intracellular signaling or by mutations of these proteins. This misregulation leads to a decay of microtubule tracks in axons, effectively reducing the number of "railway tracks" available for molecular-motor-assisted transport of intracellular organelles. In this paper, the decay of microtubule tracks is modeled by a reduction of the number density of microtubules in the central part of the axon. Simulation results indicate that the model predicts the build-up of the bell-shaped concentration wave, as the wave approaches the bottleneck (blockage) region. This increase in concentration will likely plug the bottleneck region resulting in a traffic jam that would hinder the slow axonal transport.
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Mehta, Arpan, Bhuvaneish Selvaraj, Owen Dando, Karen Burr, Giles Hardingham, and Siddharthan Chandran. "229 Dysregulated axonal homeostasis in C9orf72 iPSC-derived motor neurones." Journal of Neurology, Neurosurgery & Psychiatry 90, no. 12 (November 14, 2019): e57.3-e57. http://dx.doi.org/10.1136/jnnp-2019-abn-2.193.

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Dysregulated axonal homeostasis is a potential pathomechanism in ALS, but its relevance to the commonest known genetic mutation in ALS – the C9orf72 repeat expansion – remains unclear. We performed unbiased transcriptomics of cell-autonomous C9orf72 motor neurone (MN) perturbations in a humanised model using patient-derived induced pluripotent stem-cell lines against an isogenic background generated by CRISPR/Cas9 and studied the functional consequences of downstream axonal hits. Differential gene expression analysis examined the intersection in differentially expressed genes between the mutant-isogene pairs, revealing 215 genes: 95 up and 120 down. Pathway analysis showed an axonal signature, with upregulation of pathways involved in cytoskeletal organisation, axon guidance, and Trk receptor signalling, and downregulation of pathways involved in the mitochondrial electron transport chain and axon guidance. Significantly dysregulated genes were confirmed using real-time quantitative PCR. This led to two hypotheses examining for aberrations in axonal length and transport. Axonal length was measured using manual tracking of SMI-312 labelled axons. Axonal transport was determined by tracking Ds-Red2 labelled mitochondrial movement using a live-imaging setup and analysed using KymoToolBox. Both axonal length and transport were reduced in the mutants compared to their isogenic counterparts. Further experiments are underway to determine whether common pharmacological manipulations can rescue both phenotypes.
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Kalinski, Ashley L., Amar N. Kar, John Craver, Andrew P. Tosolini, James N. Sleigh, Seung Joon Lee, Alicia Hawthorne, et al. "Deacetylation of Miro1 by HDAC6 blocks mitochondrial transport and mediates axon growth inhibition." Journal of Cell Biology 218, no. 6 (May 8, 2019): 1871–90. http://dx.doi.org/10.1083/jcb.201702187.

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Inhibition of histone deacetylase 6 (HDAC6) was shown to support axon growth on the nonpermissive substrates myelin-associated glycoprotein (MAG) and chondroitin sulfate proteoglycans (CSPGs). Though HDAC6 deacetylates α-tubulin, we find that another HDAC6 substrate contributes to this axon growth failure. HDAC6 is known to impact transport of mitochondria, and we show that mitochondria accumulate in distal axons after HDAC6 inhibition. Miro and Milton proteins link mitochondria to motor proteins for axon transport. Exposing neurons to MAG and CSPGs decreases acetylation of Miro1 on Lysine 105 (K105) and decreases axonal mitochondrial transport. HDAC6 inhibition increases acetylated Miro1 in axons, and acetyl-mimetic Miro1 K105Q prevents CSPG-dependent decreases in mitochondrial transport and axon growth. MAG- and CSPG-dependent deacetylation of Miro1 requires RhoA/ROCK activation and downstream intracellular Ca2+ increase, and Miro1 K105Q prevents the decrease in axonal mitochondria seen with activated RhoA and elevated Ca2+. These data point to HDAC6-dependent deacetylation of Miro1 as a mediator of axon growth inhibition through decreased mitochondrial transport.
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Sleigh, James N., Alessio Vagnoni, Alison E. Twelvetrees, and Giampietro Schiavo. "Methodological advances in imaging intravital axonal transport." F1000Research 6 (March 1, 2017): 200. http://dx.doi.org/10.12688/f1000research.10433.1.

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Axonal transport is the active process whereby neurons transport cargoes such as organelles and proteins anterogradely from the cell body to the axon terminal and retrogradely in the opposite direction. Bi-directional transport in axons is absolutely essential for the functioning and survival of neurons and appears to be negatively impacted by both aging and diseases of the nervous system, such as Alzheimer’s disease and amyotrophic lateral sclerosis. The movement of individual cargoes along axons has been studied in vitro in live neurons and tissue explants for a number of years; however, it is currently unclear as to whether these systems faithfully and consistently replicate the in vivo situation. A number of intravital techniques originally developed for studying diverse biological events have recently been adapted to monitor axonal transport in real-time in a range of live organisms and are providing novel insight into this dynamic process. Here, we highlight these methodological advances in intravital imaging of axonal transport, outlining key strengths and limitations while discussing findings, possible improvements, and outstanding questions.
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Takihara, Yuji, Masaru Inatani, Kei Eto, Toshihiro Inoue, Alexander Kreymerman, Seiji Miyake, Shinji Ueno, et al. "In vivo imaging of axonal transport of mitochondria in the diseased and aged mammalian CNS." Proceedings of the National Academy of Sciences 112, no. 33 (August 3, 2015): 10515–20. http://dx.doi.org/10.1073/pnas.1509879112.

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The lack of intravital imaging of axonal transport of mitochondria in the mammalian CNS precludes characterization of the dynamics of axonal transport of mitochondria in the diseased and aged mammalian CNS. Glaucoma, the most common neurodegenerative eye disease, is characterized by axon degeneration and the death of retinal ganglion cells (RGCs) and by an age-related increase in incidence. RGC death is hypothesized to result from disturbances in axonal transport and in mitochondrial function. Here we report minimally invasive intravital multiphoton imaging of anesthetized mouse RGCs through the sclera that provides sequential time-lapse images of mitochondria transported in a single axon with submicrometer resolution. Unlike findings from explants, we show that the axonal transport of mitochondria is highly dynamic in the mammalian CNS in vivo under physiological conditions. Furthermore, in the early stage of glaucoma modeled in adult (4-mo-old) mice, the number of transported mitochondria decreases before RGC death, although transport does not shorten. However, with increasing age up to 23–25 mo, mitochondrial transport (duration, distance, and duty cycle) shortens. In axons, mitochondria-free regions increase and lengths of transported mitochondria decrease with aging, although totally organized transport patterns are preserved in old (23- to 25-mo-old) mice. Moreover, axonal transport of mitochondria is more vulnerable to glaucomatous insults in old mice than in adult mice. These mitochondrial changes with aging may underlie the age-related increase in glaucoma incidence. Our method is useful for characterizing the dynamics of axonal transport of mitochondria and may be applied to other submicrometer structures in the diseased and aged mammalian CNS in vivo.
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Cavalli, Valeria, Pekka Kujala, Judith Klumperman, and Lawrence S. B. Goldstein. "Sunday Driver links axonal transport to damage signaling." Journal of Cell Biology 168, no. 5 (February 28, 2005): 775–87. http://dx.doi.org/10.1083/jcb.200410136.

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Neurons transmit long-range biochemical signals between cell bodies and distant axonal sites or termini. To test the hypothesis that signaling molecules are hitchhikers on axonal vesicles, we focused on the c-Jun NH2-terminal kinase (JNK) scaffolding protein Sunday Driver (syd), which has been proposed to link the molecular motor protein kinesin-1 to axonal vesicles. We found that syd and JNK3 are present on vesicular structures in axons, are transported in both the anterograde and retrograde axonal transport pathways, and interact with kinesin-I and the dynactin complex. Nerve injury induces local activation of JNK, primarily within axons, and activated JNK and syd are then transported primarily retrogradely. In axons, syd and activated JNK colocalize with p150Glued, a subunit of the dynactin complex, and with dynein. Finally, we found that injury induces an enhanced interaction between syd and dynactin. Thus, a mobile axonal JNK–syd complex may generate a transport-dependent axonal damage surveillance system.
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Kar, Amar N., Seung Joon Lee, and Jeffery L. Twiss. "Expanding Axonal Transcriptome Brings New Functions for Axonally Synthesized Proteins in Health and Disease." Neuroscientist 24, no. 2 (June 8, 2017): 111–29. http://dx.doi.org/10.1177/1073858417712668.

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Intra-axonal protein synthesis has been shown to play critical roles in both development and repair of axons. Axons provide long-range connectivity in the nervous system, and disruption of their function and/or structure is seen in several neurological diseases and disorders. Axonally synthesized proteins or losses in axonally synthesized proteins contribute to neurodegenerative diseases, neuropathic pain, viral transport, and survival of axons. Increasing sensitivity of RNA detection and quantitation coupled with methods to isolate axons to purity has shown that a surprisingly complex transcriptome exists in axons. This extends across different species, neuronal populations, and physiological conditions. These studies have helped define the repertoire of neuronal mRNAs that can localize into axons and imply previously unrecognized functions for local translation in neurons. Here, we review the current state of transcriptomics studies of isolated axons, contrast axonal mRNA profiles between different neuronal types and growth states, and discuss how mRNA transport into and translation within axons contribute to neurological disorders.
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Brown, Anthony, Lei Wang, and Peter Jung. "Stochastic Simulation of Neurofilament Transport in Axons: The “Stop-and-Go” Hypothesis." Molecular Biology of the Cell 16, no. 9 (September 2005): 4243–55. http://dx.doi.org/10.1091/mbc.e05-02-0141.

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According to the “stop-and-go” hypothesis of slow axonal transport, cytoskeletal and cytosolic proteins are transported along axons at fast rates but the average velocity is slow because the movements are infrequent and bidirectional. To test whether this hypothesis can explain the kinetics of slow axonal transport in vivo, we have developed a stochastic model of neurofilament transport in axons. We propose that neurofilaments move in both anterograde and retrograde directions along cytoskeletal tracks, alternating between short bouts of rapid movement and short “on-track” pauses, and that they can also temporarily disengage from these tracks, resulting in more prolonged “off-track” pauses. We derive the kinetic parameters of the model from a detailed analysis of the moving and pausing behavior of single neurofilaments in axons of cultured neurons. We show that the model can match the shape, velocity, and spreading of the neurofilament transport waves obtained by radioisotopic pulse labeling in vivo. The model predicts that axonal neurofilaments spend ∼8% of their time on track and ∼97% of their time pausing during their journey along the axon.
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Dissertations / Theses on the topic "Axonal transport"

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Whiteley, S. J. "Axonal transport in experimental diabetes." Thesis, University of Nottingham, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.372015.

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Thornhill, Paul. "Neurofilament phosphorylation and axonal transport." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272216.

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Moutaux, Eve. "Régulation du transport axonal par l'activité neuronale : Implication pour le développement des réseaux neuronaux Neuronal activity recruits an axon-resident pool of secretory vesicles to regulate axon branching Reconstituting Corticostriatal Network on-a-Chip Reveals the Contribution of the Presynaptic Compartment to Huntington’s Disease Neuronal network maturation differently affects secretory vesicles and mitochondria transport in axons ALG-2 interacting protein-X (Alix) is required for activity-dependent bulk endocytosis at brain synapses An integrated microfluidic/microelectrode array for the study of activity-dependent intracellular dynamics in neuronal networks." Thesis, Université Grenoble Alpes, 2020. https://thares.univ-grenoble-alpes.fr/2020GRALV024.pdf.

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Pendant le développement, les projections axonales à longue distance se ramifient pour se connecter à leurs cibles. L’établissement et le remodelage de ces connexions est notamment régulé par l’activité neuronale. L’adaptation de la morphologie de l’axone nécessite alors des quantités importantes de matériel sécrétoire et de facteur trophiques comme le BDNF (brain derived neurotrophic factor). Ce matériel est transporté dans des vésicules le long de l’axone depuis le corps cellulaire où il est synthétisé, vers les sites actifs à l’extrémité de l’axone. Si le relargage de vésicules sécrétoires à la synapse est bien étudié, les mécanismes régulant le transport axonal par l’activité sont encore méconnus.Dans ce travail de thèse, nous avons dans un premier temps développé des outils permettant d’étudier les dynamiques intracellulaires dans des réseaux neuronaux. Nous avons ainsi développé une chambre microfluidique permettant de reconstruire in vitro des réseaux neuronaux physiologiques et compatibles avec de la vidéomicroscopie à haute résolution. Nous avons caractérisé l’établissement et la maturation du réseau et validé l’intérêt de ce dispositif microfluidique dans le contexte de la maladie de Huntington. Nous avons ensuite étudié l’évolution des dynamiques intracellulaires avec la maturation du réseau. Nous avons notamment observé une augmentation du transport axonal de vésicules sécrétoires en fonction de l'état de maturation du réseau neuronal. Ces premières observations ont renforcé l’hypothèse d’une régulation directe du transport axonal de vésicules sécrétoires par l’activité neuronale au cours du développement du réseau.Nous avons ainsi fait évoluer la plateforme microfluidique par l’ajout d’un réseau d’électrodes (MEA) qui permet d'étudier les dynamiques intracellulaires tout en contrôlant l’activité neuronale. A l’aide de ce système, nous avons identifié un groupe de vésicules sécrétoires ancré le long de l’axone et recruté en réponse à une haute activité neuronale en direction des sites présynaptiques actifs. Nous avons alors identifié les acteurs impliqués dans ce mécanisme dépendant de l’activité. Nous avons montré que la myosine Va permettait l’attachement des vésicules le long de l’axone dans des structures d’actine dynamique. L’activité neuronale induit une augmentation de calcium le long de l’axone, via l’activation des canaux calciques dépendant du voltage, qui régule la myosine Va et entraine le recrutement des vésicules stockées dans l’axone sur les microtubules. Une fois les acteurs identifiés, nous avons pu mettre en évidence le rôle de ce mécanisme dépendant de l’activité dans la formation de branches axonales pendant le développement. Enfin, nous avons confirmé l’existence de ce groupe de vésicules dépendant de l’activité et résidant dans l’axone in vivo grâce à la mise au point d'un système d’étude du transport axonal sur tranches aigües de cerveau en microscopie biphotonique.L’ensemble de ce travail propose de nouveaux outils in vitro et in vivo pour comprendre les régulations des dynamiques intracellulaires dans des réseaux neuronaux physiologiques. Grâce à ces outils, nous avons identifié un mécanisme de régulation local qui permet l'adressage rapide de facteurs trophiques vers les branches en développement en réponse à l’activité neuronale
During postnatal development, long-distance axonal projections form branches to connect with their targets. Establishment and remodeling of these projections are tightly regulated by neuronal activity and require a large amount of secretory material and trophic factors, such as brain derived neurotrophic factor (BDNF). Axonal transport is responsible for addressing trophic factors packed into vesicles to high demand sites where mechanisms of secretion are well-known. However, mechanisms controlling the preferential targeting of axonal vesicles to active sites in response to neuronal activity are unknown.In this work, we first developed tools to study intracellular dynamics in neuronal networks. We thus developed a microfluidic chamber to reconstruct physiologically-relevant networks in vitro which is compatible with high resolution videomicroscopy. We characterized the formation and maturation of reconstructed networks and we validated the relevance of the microfluidic platform in the context of Huntington’s disease. We then studied the evolution of intracellular dynamics with the maturation of reconstructed neuronal networks in microfluidic chambers. We observed an increase of anterograde axonal transport of secretory vesicles during maturation. These first results lead us to think that neuronal activity could regulate axonal transport of secretory vesicles over maturation of the network.Therefore, we improved the in vitro microfluidic system with a designed microelectrode array (MEA) substrate allowing us to record intracellular dynamics while controlling neuronal activity. Using this system, we identified an axon-resident reserve pool of secretory vesicles recruited upon neuronal activity to rapidly distribute secretory materials to presynaptic sites. We identified the activity-dependent mechanism of recruitment of this axonal pool of vesicles along the axon shaft. We showed that Myosin Va ensures the tethering of vesicles in the axon shaft in axonal actin structures. Specifically, neuronal activity induces a calcium increase after activation of Voltage Gated Calcium Channels along the axon, which regulates Myosin Va and triggers the recruitment of tethered vesicles on microtubules. We then showed the involvement of this activity-dependent pool for axon branches formation during axon development. By developing 2-photon live microscopy of axonal transport in acute slices, we finally confirmed that a pool of axon-resident static vesicles is recruited by neuronal activity in vivo with a similar kinetic.Altogether, this work provides new in vitro and in vivo tools to study intracellular dynamics in physiological networks. Using these tools, we identified the existence of a local mechanism of axonal transport regulation along the axon shaft, allowing rapid supply of trophic factors to developing branches
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Robinson, J. P. "Axonal transport in experimental diabetes mellitus." Thesis, University of Nottingham, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.379276.

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Tennant, Maria Elizabeth. "Axonal transport in motor neurone disease." Thesis, King's College London (University of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424667.

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Haghnia, Marjan. "Analysis of axonal transport mutants in Drosophila /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2003. http://wwwlib.umi.com/cr/ucsd/fullcit?p3091330.

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Hares, Kelly Marie. "Analysis of axonal transport deficits in multiple sclerosis." Thesis, University of Bristol, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.633448.

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Multiple sclerosis (MS) is a complex disease combining both inflammatory and neurodegenerative mechanisms. Current treatments available to MS sufferers all focus on immunosuppression. However, emerging evidence reveals axonal loss taking place alongside inflammation, suggesting protection of axons and subsequent prevention of neuronal loss is a necessary tool for future MS treatments. Mechanisms of axonal injury remain unknown, but dysregulation of axonal transport mechanisms may be important. The aim of this project was to further elucidate the role of axonal transport, including both motor proteins and associated cargoes, in axonal structure and function and to assess the effects of any changes in axonal transport mechanisms in relevance to MS disease pathology. Results from experiments performed in this thesis have shown dose dependent reductions in neurofilament (NF) phosphorylation in axons exposed to inflammatory-mediated reactive oxygen species, nitric oxide (NO). Furthermore, in MS tissue, we have seen reductions in mRNA and protein of kinesin superfamily proteins (KIFs), which are important in maintaining anterograde axonal transport. Lastly, in vitro studies using rat cortical neurons have shown reduced KIFSA and KIF21B gene expression significantly reduces neuronal viability. Phosphorylated neurofilaments (pNFs) are vital in maintaining axonal integrity and function. ,Dysregulation of anterograde axonal motor proteins including, KIFSA, KIF21B and KIF1B is likely to result in reduced transport of structural cytoskeletal components such as p-NFs, compromising axonal structure and integrity, as seen in many neurodegenerative diseases. Therefore, preservation of axonal transport mechanisms and neurofilament phosphorylation may be a potential therapeutic avenue to explore to protect against on-going neurodegeneration in MS and other neurological diseases. Overall, the results presented here offer more insight into the neurodegenerative processes occurring in MS. However, further studies are required to ascertain the direct functional consequences of reduced KIF gene/protein expression on axonal transport and funct ion in the disease course.
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Archer, D. R. "Axonal transport and related responses to nerve injury." Thesis, University of Liverpool, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234835.

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Hill, Josephine Elizabeth. "Investigating mechanisms involved in α-synuclein axonal transport." Thesis, King's College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407861.

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Weiss, Kurt R. "The role of Huntingtin in fast axonal transport." Thesis, Massachusetts Institute of Technology, 2012. http://hdl.handle.net/1721.1/70106.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2012.
This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged from student-submitted PDF version of thesis.
Includes bibliographical references.
Huntington's Disease (HD) is an autosomal dominant, neurodegenerative disease that occurs when an expansion of the polyQ tract of the huntingtin gene expands to greater than ~35 residues. This mutation leads to aggregation of the Huntingtin protein (Htt) and degeneration of striatal and cortex neurons, ultimately causing motor impairment and personality changes. Neither the mechanism by which mutant Htt causes toxicity, nor the endogenous function of wild-type Htt, are well understood. To explore mechanisms of mutant Htt-induced toxicity, we generated and characterized a Drosophila model of HD by expressing a 588 amino acid N-terminal fragment of human Htt with 138 glutamines, and tagged with mRFP (Q138Htt-RFP). We used this model to conduct a screen for genes that modify cytoplasmic aggregation and/or toxicity phenotypes. We identified two classes of interacting suppressors in our screen: those that rescue viability while decreasing Htt expression and aggregation, and those that rescue viability independent of effects on Htt aggregation, suggesting that aggregation and toxicity can be separated. To evaluate the putative function of Htt in fast axonal transport, we characterized the co-localization of the Drosophila Htt homolog tagged with mRFP (dHtt-RFP), and the alterations in axonal transport kinetics associated with a dhtt null. We find that dHtt co-localizes with a subset of cargos including synaptic vesicles and mitochondria, and acts locally on these cargos to increase transport processivity. Finally, we evaluated the effects of Q138Htt-RFP expression on transport kinetics. We find that the majority of transport cargos bypass Q138Htt aggregates, indicating they are not complete blockages of axonal transport. We also observe reduced mitochondrial transport in the absence of aggregates, suggesting aggregate-independent transport defects. Our observations of transport in vivo support a role for wild-type Htt in mediating fast axonal transport of membrane bound organelles, and suggest that mutant Htt can cause aggregation-dependent and -independent defects in axonal transport.
by Kurt R. Weiss.
Ph.D.
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Books on the topic "Axonal transport"

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Vagnoni, Alessio, ed. Axonal Transport. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1990-2.

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1933-, Smith Richard S., Bisby Mark A, and International Union of Physiological Sciences Congress, eds. Axonal transport: Proceedings of a satellite symposium of the 30th Congress of the International Union of Physiological Sciences held at the University of Calgary, Alberta, Canada, July 9-12, 1986. New York: Liss, 1987.

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1941-, Iqbal Zafar, ed. Axoplasmic transport. Boca Raton, Fla: CRC Press, 1986.

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Oterendorp, Christian ˜vanœ. Quantification of retrograde axonal transport in the rat optic nerve by Fluorogold spectrometry. Freiburg: Universität, 2012.

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Brown, A. M. Ionic mechanisms of aglycemic axon injury in mammalian central white mater. Philadelphia, Penn: Lippincott Williams & Wilkins, Inc., 2001.

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Brown, A. M. Metabolic substrates other than glucose support axon function in central white mater. New York, N.Y: Wiley-Liss, Inc., 2001.

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A, Lappi Douglas, ed. Suicide transport and immunolesioning. Austin: R.G. Landes, 1994.

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Gajdusek, D. Carleton. Interference with axonal transport of neurofilament as the common etiology and pathogenesis of neurofibrillary tangles, amyotrophic lateral sclerosis, parkinsonism-dementia, and many other degenerations of the CNS: A series of hypotheses, perspectives for research. Bethesda, Md: U.S. Dept. of Health and Human Services, National Institutes of Health, Laboratory of Central Nervous System Studies, National Institute of Neurological and Communicative Disorders and Stroke, 1985.

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Simard, Alain. Disruption of sciatic nerve axon transport inhibits skeletal muscle fiber growth. Sudbury, Ont: Laurentian University, 2000.

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(Editor), Richard S. Smith, and Mark A. Bisby (Editor), eds. Axonal Transport. John Wiley & Sons, 1987.

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Book chapters on the topic "Axonal transport"

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Takihara, Yuji, and Masaru Inatani. "Axonal Transport." In Neuroprotection and Neuroregeneration for Retinal Diseases, 133–41. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54965-9_10.

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Brown, Anthony. "Axonal Transport." In Neuroscience in the 21st Century, 333–79. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3474-4_14.

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Brown, Anthony. "Axonal Transport." In Neuroscience in the 21st Century, 1–47. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6434-1_14-3.

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Brown, Anthony. "Axonal Transport." In Neuroscience in the 21st Century, 607–52. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-88832-9_14.

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Brown, Anthony. "Axonal Transport." In Neuroscience in the 21st Century, 255–308. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-1997-6_14.

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Mehta, Arpan R., Siddharthan Chandran, and Bhuvaneish T. Selvaraj. "Assessment of Mitochondrial Trafficking as a Surrogate for Fast Axonal Transport in Human Induced Pluripotent Stem Cell–Derived Spinal Motor Neurons." In Methods in Molecular Biology, 311–22. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1990-2_16.

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AbstractAxonal transport is essential for the development, function, and survival of the nervous system. In an energy-demanding process, motor proteins act in concert with microtubules to deliver cargoes, such as organelles, from one end of the axon to the other. Perturbations in axonal transport are a prominent phenotype of many neurodegenerative diseases, including amyotrophic lateral sclerosis. Here, we describe a simple method to fluorescently label mitochondrial cargo, a surrogate for fast axonal transport, in human induced pluripotent stem cell–derived motor neurons. This method enables the sparse labeling of axons to track directionality of movement and can be adapted to assess not only the cell autonomous effects of a genetic mutation on axonal transport but also the cell non-autonomous effects, through the use of conditioned medium and/or co-culture systems.
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McLean, W. Graham, Martin Frizell, and Johan Sjöstrand. "Pathology of Axonal Transport." In Alterations of Metabolites in the Nervous System, 67–86. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4757-6740-7_3.

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Willis, Dianna E., and Jeffery L. Twiss. "Profiling Axonal mRNA Transport." In Methods in Molecular Biology, 335–52. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-005-8_21.

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Shekari, Arman, and Margaret Fahnestock. "Retrograde Axonal Transport of Neurotrophins in Basal Forebrain Cholinergic Neurons." In Methods in Molecular Biology, 249–70. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1990-2_13.

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AbstractAxonal transport is key for the survival and function of all neurons. This process is especially important in basal forebrain cholinergic neurons due to their extremely long and diffuse axonal projections. These neurons are critical for learning and memory and degenerate rapidly in age-related neurodegenerative disorders like Alzheimer’s and Parkinson’s disease. The vulnerability of these neurons to age-related neurodegeneration may be partially attributed to their reliance on retrograde axonal transport for neurotrophic support. Unfortunately, little is known about the molecular biology underlying the retrograde transport dynamics of these neurons due to the difficulty associated with their maintenance in vitro. Here, we outline a protocol for culturing primary rodent basal forebrain cholinergic neurons in microfluidic chambers, devices designed specifically for the study of axonal transport in vitro. We outline protocols for labeling neurotrophins and tracking neurotrophin transport in these neurons. Our protocols can also be used to study axonal transport in other types of primary neurons such as cortical and hippocampal neurons.
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Moya, Kenneth L. "Retinal Ganglion Cell Axonal Transport." In Development and Organization of the Retina, 259–74. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5333-5_14.

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Conference papers on the topic "Axonal transport"

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Kuznetsov, A. V., A. A. Avramenko, and D. G. Blinov. "Simulation of Traffic Jam Formation in Fast Axonal Transport." In ASME 2009 Heat Transfer Summer Conference collocated with the InterPACK09 and 3rd Energy Sustainability Conferences. ASMEDC, 2009. http://dx.doi.org/10.1115/ht2009-88345.

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Many neurodegenerative diseases, such as Alzheimer’s disease, are linked to swellings occurring in long arms of neurons. Many scientists believe that these swellings result from traffic jams caused by the failure of intracellular machinery responsible for fast axonal transport; such traffic jam can plug an axon and prevent the sufficient amount of organelles to be delivered toward the synapse of the axon. Mechanistic explanation of the formation of traffic jams in axons induced by overexpression of tau protein is based on the hypothesis that the traffic jam is caused not by the failure of molecular motors to transport organelles along individual microtubules but rather by the disruption of the microtubule system in an axon, by the formation of a swirl of disoriented microtubules at a certain location in the axon. This paper investigates whether a microtubule swirl itself, without introducing into the model microtubule discontinuities in the traffic jam region, is capable of capturing the traffic jam formation. The answer to this question can provide important insight into the mechanics of the formation of traffic jams in axons.
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Beiu, Valeriu, Noemi Clara Rohatinovici, Leonard Daus, and Valentina Emilia Balas. "Transport reliability on axonal cytoskeleton." In 2017 14th International Conference on Engineering of Modern Electric Systems (EMES). IEEE, 2017. http://dx.doi.org/10.1109/emes.2017.7980404.

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Kuznetsov, A. V. "Modeling Mass Transport in Axonal Transport Drug Delivery." In ASME 2012 Heat Transfer Summer Conference collocated with the ASME 2012 Fluids Engineering Division Summer Meeting and the ASME 2012 10th International Conference on Nanochannels, Microchannels, and M. ASME, 2012. http://dx.doi.org/10.1115/ht2012-58025.

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Mudrakola, Harsha V., Chengbiao Wu, Kai Zhang, and Bianxiao Cui. "Single Molecule Imaging of Axonal Transport in Live Neurons." In Laser Science. Washington, D.C.: OSA, 2009. http://dx.doi.org/10.1364/ls.2009.lsthb3.

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Melkikh, A. V., M. I. Sutormina, S. G. Babajanyan, and E. A. Zafirov. "A model of microfilaments: Myosin movement and axonal transport." In PHYSICS, TECHNOLOGIES AND INNOVATION (PTI-2019): Proceedings of the VI International Young Researchers’ Conference. AIP Publishing, 2019. http://dx.doi.org/10.1063/1.5134340.

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Chen, Tong, Chenzlei Peng, Ming Li, Xudong Chen, Sidan Du, and Yang Li. "A Review on Quantitative Analyzing Axonal Transport of Mitochondria." In 2021 IEEE 3rd Global Conference on Life Sciences and Technologies (LifeTech). IEEE, 2021. http://dx.doi.org/10.1109/lifetech52111.2021.9391884.

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Nair, Alka, Shikha Ahlawat, Sandhya P. Koushika, Niranjan Joshi, and Mohanasankar Sivaprakasam. "Computer assisted analysis of axonal transport velocities from kymographs." In 2014 International Conference on Signal Processing and Communications (SPCOM). IEEE, 2014. http://dx.doi.org/10.1109/spcom.2014.6983977.

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"Nanoparticle axonal transport assessment in neurodegeneration susceptible mice strain." In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-418.

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Migazzi, Alice, Chiara Scaramuzzino, Eric Anderson, Debasmita Tripathy, Ivó H. Hernández, Rogan Grant, Michela Roccuzzo, et al. "A11 Huntingtin-mediated axonal transport requires arginine methylation by PRMT6." In EHDN Abstracts 2021. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/jnnp-2021-ehdn.10.

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Qiu, Minhua, Hao-Chih Lee, and Ge Yang. "Nanometer resolution tracking and modeling of bidirectional axonal cargo transport." In 2012 IEEE 9th International Symposium on Biomedical Imaging (ISBI 2012). IEEE, 2012. http://dx.doi.org/10.1109/isbi.2012.6235724.

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Reports on the topic "Axonal transport"

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Baas, Peter W. Studies on Axonal Transport in an Animal Model for Gulf War Syndrome. Fort Belvoir, VA: Defense Technical Information Center, July 2008. http://dx.doi.org/10.21236/ada486927.

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Narayanan, Vinodh. Studies of Kinesins and Axonal Transport in a Mouse Model of NF1. Fort Belvoir, VA: Defense Technical Information Center, March 2008. http://dx.doi.org/10.21236/ada481962.

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Terry, Alvin V. Organophosphate-Related Alterations in Myelin and Axonal Transport in the Living Mammalian Brain. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613306.

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Terry, Alvin V. Organophosphate-Related Alterations in Myelin and Axonal Transport in the Living Mammalian Brain. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada596490.

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