Relevant bibliographies by topics / Neurotrophins

Academic literature on the topic 'Neurotrophins'

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Published: 4 June 2021
Last updated: 23 February 2023

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Journal articles on the topic "Neurotrophins"

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Gupta, Akash, Jeremias G. Galletti, Zhiyuan Yu, Kevin Burgess, and Cintia S. de Paiva. "A, B, C’s of Trk Receptors and Their Ligands in Ocular Repair." International Journal of Molecular Sciences 23, no. 22 (November 15, 2022): 14069. http://dx.doi.org/10.3390/ijms232214069.

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Neurotrophins are a family of closely related secreted proteins that promote differentiation, development, and survival of neurons, which include nerve growth factor (NGF), brain-derived neurotrophic factor, neurotrophin-3, and neurotrophin-4. All neurotrophins signal through tropomyosin receptor kinases (TrkA, TrkB, and TrkC) which are more selective to NGF, brain-derived neurotrophic factor, and neurotrophin-3, respectively. NGF is the most studied neurotrophin in the ocular surface and a human recombinant NGF has reached clinics, having been approved to treat neurotrophic keratitis. Brain-derived neurotrophic factor, neurotrophin-3, and neurotrophin-4 are less studied neurotrophins in the ocular surface, even though brain-derived neurotrophic factor is well characterized in glaucoma, retina, and neuroscience. Recently, neurotrophin analogs with panTrk activity and TrkC selectivity have shown promise as novel drugs for treating dry eye disease. In this review, we discuss the biology of the neurotrophin family, its role in corneal homeostasis, and its use in treating ocular surface diseases. There is an unmet need to investigate parenteral neurotrophins and its analogs that activate TrkB and TrkC selectively.
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Krüttgen, Alex, J. Carsten Möller, John V. Heymach, and Eric M. Shooter. "Neurotrophins induce release of neurotrophins by the regulated secretory pathway." Proceedings of the National Academy of Sciences 95, no. 16 (August 4, 1998): 9614–19. http://dx.doi.org/10.1073/pnas.95.16.9614.

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Recent studies have established that neurotrophin synthesis and secretion are regulated by activity and that these factors are involved in activity-dependent processes in the nervous system. Neurotrophins also are known to induce increases in intracellular calcium, a trigger for regulated secretion. This finding raises the possibility that neurotrophins themselves may stimulate regulated secretion of neurotrophins. To address this question, we studied the release of neurotrophins from transfected PC12 cells, a widely used model for neuronal secretion and neurotrophin signal transduction. We found that neurotrophins induced the regulated secretion of brain-derived neurotrophic factor, neurotrophin-3 (NT-3), and neurotrophin-4/5. The effect of brain-derived neurotrophic factor on release of NT-3 could be abolished by REX, a p75 blocking antibody, but not by K252a, an inhibitor of neurotrophin tyrosine kinase receptor (Trk) signaling. The nerve growth factor effect on release of NT-3 could be blocked only by simultaneous application of REX and K252a, suggesting that they are mediated by TrkA as well as p75. Our data show that neurotrophins are able to induce the regulated secretion of neurotrophins and suggest a signal-transducing role for both TrkA and p75 in this process. The neurotrophin-induced release of neurotrophins may be relevant for activity-dependent processes such as synaptic plasticity and memory formation.
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Dechant, G., S. Biffo, H. Okazawa, R. Kolbeck, J. Pottgiesser, and Y. A. Barde. "Expression and binding characteristics of the BDNF receptor chick trkB." Development 119, no. 2 (October 1, 1993): 545–58. http://dx.doi.org/10.1242/dev.119.2.545.

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Previous studies using transfected cells have indicated that the mammalian receptor tyrosine kinase trkB binds the neurotrophins brain-derived neurotrophic factor, neurotrophin-3 and neurotrophin-4. However, most studies demonstrating that these neurotrophins prevent the death of embryonic neurons and have specific neuronal receptors have been performed with chick neurons. In order to explore the possibility that trkB is the molecular entity representing the high-affinity receptor for brain-derived neurotrophic factor on embryonic chick neurons, we cloned and expressed a chick trkB cDNA. In situ hybridisation results indicate that the distribution of trkB mRNA in the peripheral nervous system of the developing chick embryo correlates well with the structures known to respond to brain-derived neurotrophic factor. Binding studies performed with a cell line stably transfected with the ctrkB cDNA indicate a dissociation constant for brain-derived neurotrophic factor of 9.9 × 10(−10) M, which is distinctly higher than that found on primary chick sensory neurons (1.5 × 10(−11) M). When binding of brain-derived neurotrophic factor was determined in the presence of other neurotrophins, neurotrophin-3 was found efficiently to prevent the binding of brain-derived neurotrophic factor to both the ctrkB cell line and embryonic sensory neurons. In vitro, neurotrophin-3 at high concentrations completely blocked the survival normally seen with brain-derived neurotrophic factor. Thus, unlike previous cases of receptor occupancy by heterologous neurotrophins (which resulted in agonistic effects), the interaction between the brain-derived neurotrophic factor receptor and neurotrophin-3 on sensory neurons is antagonistic.
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YIN, Q., G. J. KEMP, and S. P. FROSTICK. "Neurotrophins, Neurones and Peripheral Nerve Regeneration." Journal of Hand Surgery 23, no. 4 (August 1998): 433–37. http://dx.doi.org/10.1016/s0266-7681(98)80117-4.

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Successful peripheral nerve regeneration requires optimal conditions both in the macro-environment and micro-environment. Many methods have been used to improve the macro-environment for the regenerating nerve. However, much less is known about the micro-environment, and in particular the complex neurochemical interactions involved. Several neurotrophic factors have been shown to play an essential trophic role in the development, maintenance and regulation of neuronal function. These include nerve growth factor (NGF) and several recently identified members of the NGF family, namely brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), neurotrophin-4/5 (NT-4/5) and neurotrophin-6 (NT-6). In this review we summarize recent studies of the effects of these neurotrophins on neurones, especially their effects on motor neurones and their axonal outgrowth. We discuss prospects for the future and point out what remains to be understood about the role of neurotrophins to enhance peripheral nerve regeneration.
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Gatta, Claudia, Valentina Schiano, Chiara Attanasio, Carla Lucini, and Antonio Palladino. "Neurotrophins in Zebrafish Taste Buds." Animals 12, no. 13 (June 23, 2022): 1613. http://dx.doi.org/10.3390/ani12131613.

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The neurotrophin family is composed of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), Neurotrophin 3 (NT3) and NT4. These neurotrophins regulate several crucial functions through the activation of two types of transmembrane receptors, namely p75, which binds all neurotrophins with a similar affinity, and tyrosine kinase (Trk) receptors. Neurotrophins, besides their well-known pivotal role in the development and maintenance of the nervous system, also display the ability to regulate the development of taste buds in mammals. Therefore, the aim of this study is to investigate if NGF, BDNF, NT3 and NT4 are also present in the taste buds of zebrafish (Danio rerio), a powerful vertebrate model organism. Morphological analyses carried out on adult zebrafish showed the presence of neurotrophins in taste bud cells of the oropharyngeal cavity, also suggesting that BDNF positive cells are the prevalent cell population in the posterior part of the oropharyngeal region. In conclusion, by suggesting that all tested neurotrophins are present in zebrafish sensory cells, our results lead to the assumption that taste bud cells in this fish species contain the same homologous neurotrophins reported in mammals, further confirming the high impact of the zebrafish model in translational research.
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Hennigan, A., R. M. O'Callaghan, and Á. M. Kelly. "Neurotrophins and their receptors: roles in plasticity, neurodegeneration and neuroprotection." Biochemical Society Transactions 35, no. 2 (March 20, 2007): 424–27. http://dx.doi.org/10.1042/bst0350424.

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It is beyond doubt that the neurotrophin family of proteins plays key roles in determining the fate of the neuron, not only during embryonic development, but also in the adult brain. Neurotrophins such as NGF (nerve growth factor) and BDNF (brain-derived neurotrophic factor) can play dual roles: first, in neuronal survival and death, and, secondly, in activity-dependent plasticity. The neurotrophins manifest their effects by binding to two discrete receptor subtypes: the Trk (tropomyosin receptor kinase) family of RTKs (receptor tyrosine kinases) and the p75NTR (p75 neurotrophin receptor). The differential activation of these receptors by the mature neurotrophins and their precursors, the proneurotrophins, renders analysis of the biological functions of these receptors in the adult brain highly complex. Here, we briefly give a broad review of current knowledge of the roles of neurotrophins in the adult brain, including expression of hippocampal plasticity, neurodegeneration and exercise-induced neuroprotection.
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Kozlov, Evgenii M., Andrey V. Grechko, Yegor S. Chegodaev, Wei-Kai Wu, and Alexander N. Orekhov. "Contribution of Neurotrophins to the Immune System Regulation and Possible Connection to Alcohol Addiction." Biology 9, no. 4 (March 28, 2020): 63. http://dx.doi.org/10.3390/biology9040063.

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The first references to neurotrophic factors date back to the middle of the 20th century when the nerve growth factor (NGF) was first discovered. Later studies delivered a large amount of data on neurotrophic factors. However, many questions regarding neurotrophin signaling still remain unanswered. One of the principal topics in neurotrophin research is their role in the immune system regulation. Another important research question is the possible involvement of neurotrophin signaling in the pathological processes associated with alcoholism. Among known neurotrophins, NT-4 remains the least studied and appears to be involved in alcoholism and chronic stress pathogenesis. In this review we discuss known neurotrophin signaling cascades mediated by different neurotrophin receptors, as well as provide a generalization of the data regarding the influence of neurotrophins NGF, BDNF, and NT-4 on the immune system and their potential contribution to the pathogenesis of alcoholism.
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Bohmwald, Karen, Catalina A. Andrade, Valentina P. Mora, José T. Muñoz, Robinson Ramírez, María F. Rojas, and Alexis M. Kalergis. "Neurotrophin Signaling Impairment by Viral Infections in the Central Nervous System." International Journal of Molecular Sciences 23, no. 10 (May 22, 2022): 5817. http://dx.doi.org/10.3390/ijms23105817.

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Neurotrophins, such as nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin 3 (NT-3), NT-4, and NT-5, are proteins involved in several important functions of the central nervous system. The activation of the signaling pathways of these neurotrophins, or even by their immature form, pro-neurotrophins, starts with their recognition by cellular receptors, such as tropomyosin receptor kinase (Trk) and 75 kD NT receptors (p75NTR). The Trk receptor is considered to have a high affinity for attachment to specific neurotrophins, while the p75NTR receptor has less affinity for attachment with neurotrophins. The correct functioning of these signaling pathways contributes to proper brain development, neuronal survival, and synaptic plasticity. Unbalanced levels of neurotrophins and pro-neurotrophins have been associated with neurological disorders, illustrating the importance of these molecules in the central nervous system. Furthermore, reports have indicated that viruses can alter the normal levels of neurotrophins by interfering with their signaling pathways. This work discusses the importance of neurotrophins in the central nervous system, their signaling pathways, and how viruses can affect them.
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Rochlitzer, S., C. Nassenstein, and A. Braun. "The contribution of neurotrophins to the pathogenesis of allergic asthma." Biochemical Society Transactions 34, no. 4 (July 21, 2006): 594–99. http://dx.doi.org/10.1042/bst0340594.

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The neurotrophins nerve growth factor, brain-derived neurotrophic factor, NT-3 (neurotrophin 3) and NT-4 are known for regulating neuron development, function and survival. Beyond this, neurotrophins were found to exert multiple effects on non-neuronal cells such as immune cells, smooth muscle and epithelial cells. In allergic asthma, airway inflammation, airway obstruction, AHR (airway hyperresponsiveness) and airway remodelling are characteristic features, indicating an intensive interaction between neuronal, structural and immune cells in the lung. In allergic asthma patients, elevated neurotrophin levels in the blood and locally in the lung are commonly observed. Additionally, structural cells of the lung and immune cells, present in the lung during airway inflammation, were shown to be capable of neurotrophin production. A functional relationship between neurotrophins and the main features of asthma was revealed, as airway obstruction, airway inflammation, AHR and airway remodelling were all shown to be stimulated by neurotrophins. The aim of the present review is to provide an overview of neurotrophin sources and target cells in the lung, concerning their possible role as mediators between structural cells, immune cells and neurons, connecting the different features of allergic asthma.
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Stein, Dan J., Willie M. U. Daniels, Jonathan Savitz, and Brian H. Harvey. "Brain-Derived Neurotrophic Factor: The Neurotrophin Hypothesis of Psychopathology." CNS Spectrums 13, no. 11 (November 2008): 945–49. http://dx.doi.org/10.1017/s1092852900013997.

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ABSTRACTWhile monoaminergic hypotheses of psychopathology remain popular, there has been growing interest in the role of neurotrophins in neuropsychiatric disorders. Basic laboratory work has documented the importance of neurotrophins in neuronal survival and synaptic plasticity, and a range of clinical studies has provided analogous evidence of their role in neuropathology. Work on gene variants in brain-derived neurotrophic factor, and associated changes in structural and function brain imaging, have further contributed to our understanding of this area. Much remains to be done to delineate fully the relevant mechanisms by which brain-derived neurotrophic factor and other neurotrophins contribute to psychopathology, and to develop targeted therapeutic interventions. Nevertheless, the neurotrophin hypothesis has already given impetus to a range of valuable research.
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Dissertations / Theses on the topic "Neurotrophins"

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Karchewski, Laurie Ann. "Neurotrophins and neurotrophin receptors in adult primary sensory neurons." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0034/NQ63884.pdf.

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Ward, Nicole L. "Neurotrophins and neurotrophin signal transduction in cholinergic neurons of the mouse forebrain." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0020/NQ49297.pdf.

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Timm, David Eugene. "Conformation, stability and interactions of the neurotrophins and the low-affinity neurotrophin receptor." Case Western Reserve University School of Graduate Studies / OhioLINK, 1993. http://rave.ohiolink.edu/etdc/view?acc_num=case1057179020.

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Coppell, Alexander. "Antidepressant interactions with neurotrophins." Thesis, University of Oxford, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.400564.

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Travaglia, Alessio. "Memory, metals and neurotrophins." Doctoral thesis, Università di Catania, 2013. http://hdl.handle.net/10761/1346.

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In the last decades, one of the main interests of neuroscientists has been to unravel the molecular mechanisms of memory. Neurotrophins are proteins involved in development and survival of neurons as well as they are active player in memory formation and synaptic plasticity. d-block biometals, especially copper and zinc, are emerging as crucial player in the physiology of the brain. As matter of fact, there is a significant overlap between brain areas in which the highest concentration of metals have been measured and those where the neurotrophins exert their biological activity. Metal ions can directly modulate their activities, through conformational changes, and/or indirectly by activating their downstream signaling in a neurotrophin-independent mode. Despite the importance of these modulations, there is the lack of experimental data regarding the coordination features of metal ions complexes with neurotrophins. The N-terminal domain of neurotrophins is critical for the binding selectivity and activation of their receptors. We synthesized the N-terminus peptide fragments encompassing the human neurotrophins, characterized their copper(II) and zinc(II) complexes by means of potentiometric, spectroscopic (UV/Vis, CD, NMR and EPR) techniques and DFT calculations, tested the metal-driven biological effect. The coordination features of acetylated as well as single point mutated peptides have been also studied to prove the involvement of each donor group. The functional interaction of biometals with neurotrophins and related peptides has been tested by biological assay on SHSY5Y neuroblastoma cell, providing evidence of the correlation between biological activity and coordination environment. Our biochemical characterizations of the neurotrophins signaling, both in vitro and in vivo, have shed some light on the possible use of neurotrophins and neurotrophins-like peptides in neurological disorders. Indeed, the use of neurotrophins in the early stages of neurodegenerative diseases has recently gained attention. However, there are limits to such therapy, e.g. insufficient permeability of the blood-brain barrier and inappropriate activation of receptors that trigger side effects. The use of peptidomimetic combined with systems that guarantee their delivery might allow to overcome these restrictions. In view of application as functional nanoplatforms for smart drug delivery, supported lipid bilayers formed by neurotrophin peptidomimetics/small unilamellar vescicles adsorption on silica (both planar model and nanoparticles) have been characterized. In conclusion, the interaction of metals and neurotrophins might represent a crossroad for neuronal physiology. Better understanding of metal ion-driven neurotrophins signal transduction and intercellular signaling, as well as vice versa, the role of neurotrophins in the control of metal ions homeostasis, could disclose helpful information and it is therefore strongly raising as one of the most critical step in the study of neurodegenerative diseases as well in the physiological mechanisms of memory.
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Marco, Salazar Paola. "The role of neurotrophins and neurotrophin receptors in the pathogenesis of neurodegeneration and neuroregeneration." Doctoral thesis, Universitat Autònoma de Barcelona, 2014. http://hdl.handle.net/10803/285547.

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Las neurotrofinas son una familia de factores de crecimiento polipeptídicos estructuralmente relacionados que influyen en el desarrollo, mantenimiento, supervivencia, reparación y muerte de las células neuronales y no neuronales en el sistema nervioso. Los miembros pertenecientes a este grupo que incluyen NGF, BDNF, NT-3 y NT 4/5, ejercen sus funciones intracelulares mediante la unión a dos tipos de receptores transmembrana muy diferentes; los receptores de tirosin quinasa (Trk A, B y C) y el receptor de neurotrofina p75 (p75NTR), un miembro perteneciente a la superfamilia del factor de necrosis tumoral (TNF). Las neurotrofinas son objeto de estudio de la investigación actual debido a su participación tanto en condiciones fisiológicas como patológicas. Estudios previos publicados señalan las neurotrofinas como agentes terapéuticos prometedores. En esta tesis, se llevó a cabo un estudio inmunohistoquímico de todas estas neurotrofinas (a excepción de NT4 / 5) y sus receptores en el sistema nervioso de diferentes modelos transgénicos murinos en dos escenarios diferentes: neurodegeneración del sistema nervioso central y neuroregeneración en el sistema nervioso periférico. Con el fin de dilucidar los mecanismos neurodegenerativos asociados a la patogénesis de las enfermedades priónicas, un modelo murino (BoTg 110) de la encefalopatía espongiforme bovina (EEB), que sobreexpresa la proteína priónica celular bovina, fué sometido a una inoculación intracerebral con un inóculo de EEB. Se evaluaron los cambios neuropatológicos en el encéfalo y se compararon con el marcaje inmunohistoquímico de las NTs/NTRs. Además, en este experimento, se incluyó un modelo “wild type” (Balb-C) como control para realizar un completo mapeo del inmunomarcaje de las NTs/NTRs en el encéfalo –normal- de ratón. Se observó una correlación entre el incremento en el marcaje inmunohistoquímico del receptor p75, especialmente en células gliales con la distribución de lesiones asociadas a la EEB. Esto podría sugerir que, entre todos los factores neurotróficos evaluados, este receptor podría está implicado en la fase terminal de la patología de la EEB. Además, el estudio del sistema nervioso periférico se llevó a cabo tras inducir experimentalmente un daño mecánico (aplastamiento o “crush”) en el nervio ciático en ratones transgénicos macho RIP-I / hIFNβ. En este modelo, el papel de las NTs/NTRs en los procesos de neuroregeneración se evaluó en el nervio, en los correspondientes ganglios de la raíz dorsal y en médula espinal a diferentes tiempos después de la cirugía. Se observaron cambios en la inmunorreactividad de todos los factores estudiados en estas tres estructuras. Observamos algunas particularidades en función del tiempo y la neurotrofina o receptor estudiado que se correspondían con la regeneración nerviosa. Nuestros resultados indicaron que, las neurotrofinas, en particular el receptor p75, podrían ser estudiadas como posibles dianas terapéuticas para el tratamiento de las enfermedades priónicas. Del mismo modo, una combinación de neurotrofinas podría ser de utilidad para tratar pacientes afectados por lesiones de nervios periféricos, ayudando así al proceso regenerativo. Profundizar en el conocimiento del papel que juegan las neurotrofinas en este contexto es indispensable para poder desarrollar tratamientos más eficaces de aquellos trastornos que afectan el sistema nervioso.
Neurotrophins (NTs) are a unique family of structurally related polypeptide growth factors that influence the development, maintenance, survival, repair and death of neuronal and non neuronal cells in the nervous system. Members belonging to this group include NGF, BDNF, NT-3 and NT 4/5. They exert their intracellular roles by binding to two different transmembrane types of receptors; the tyrosine kinase receptors (Trk A, B and C) and the p75 neurotrophin receptor (p75NTR), a member of the tumor necrosis factor receptor (TNF) superfamily. Neurotrophins are under current investigation for their involvement in physiological and pathological conditions. Previously published literature points them out as promising therapeutic agents. In this thesis, an immunohistochemical assessment of all these neurotrophins (with the exception of NT4/5) and their receptors was performed in the nervous system of different adult transgenic murine models in two different scenarios: central nervous system neurodegeneration and peripheral nervous system neuroregeneration. In order to determine the role of NTs/NTRs in the neurodegenerative mechanisms associated to prion diseases pathogenesis, the BoTg 110, a murine model of bovine spongiform encephalopathy (BSE), which overexpresses the bovine prion cellular protein, was subjected to an intracerebral inoculation with a BSE isolate. Neuropathological features where assessed and compared to NTs/NTRs immunolabelling. Furthermore, in this experiment, a wild type mouse line (Balb-C) was included as a control for a thorough -normal- mouse brain mapping of the NTs/NTRs immunolabelling. An increased expression of p75NTR, particularly in glial cells, was observed to correlate well with TSE related lessions. This may suggest that, among all neurotrophic factors evaluated, this receptor is involved in end stage brain pathology in BSE. Additionally, the study of the peripheral nervous system neuroregeneration was carried out following an experimental unilateral mechanic injury (crush) in the sciatic nerve of male transgenic RIP-I/hIFNβ mice. In this model, the involvement of NTs/NTRs in the neuroregenerative process was evaluated in the nerve, in the corresponding dorsal root ganglia and in the lumbar spinal cord segments at different time points after surgery. Our findings indicated changes in the immunoreactivity for all factors studied in these three structures. Particularities depending on the time point and studied NTs were observed related to the neuroregenerative processes Our results indicate that neurotrophins, and particularly the p75NTR could be further studied as possible therapeutic targets for prion diseases. Likewise, combined neurotrophins could be useful to treat patients affected by peripheral nerve injuries and therefore contributing to the peripheral nerve regeneration.A better understand ing of the mechanisms underlying the neutrophin function involvement is a prerequisite for the development of more effective treatments for the disorders affecting the nervous system
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Lichtenecker, Petra [Verfasser]. "Modulation der Sekretion des Neurotrophins "Brain-Derived Neurotrophic Factor" durch zyklisches Adenosinmonophosphat / Petra Lichtenecker." Magdeburg : Universitätsbibliothek, 2016. http://d-nb.info/1128726483/34.

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Agerman, Karin. "Specificity of neurotrophins in the nervous system : a genetic approach to determine receptor engagement by neurotrophins /." Stockholm, 2003. http://diss.kib.ki.se/2004/91-7349-730-4/.

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Watson, Judy J. "Neurotrophins and their receptors as therapeutics." Thesis, University of Bristol, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.431610.

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Mazouffre, Clément. "Rôles du couple TrkB/BDNF et de l’autophagie dans la survie de cellules de cancer colorectal." Thesis, Limoges, 2016. http://www.theses.fr/2016LIMO0091/document.

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Le cancer colorectal (CCR) est le premier cancer digestif dans les pays occidentaux. Malgré les progrès thérapeutiques réalisés au cours des deux dernières décennies, la survie relative à 5 ans ne dépasse pas 56%, et s’abaisse à 11,3% pour les patients métastatiques. Le pronostic est lié au stade de développement de la maladie au moment du diagnostic. Les décès sont en rapport avec une résistance primaire de la masse tumorale aux thérapies, ou la survenue de récidive, en rapport avec une maladie microscopique résiduelle, non contrôlée par les thérapies systémiques adjuvantes. Le travail réalisé au sein de notre laboratoire portant sur deux voies de signalisation met en leurs rôles dans le CCR : les neurotrophines (NTs, facteurs de croissance impliqués dans la survie des cellules cancéreuses) et l’autophagie (processus de recyclage cellulaire impliqué dans la résistance au stress). Le but de cette étude a été d’analyser la part de ces deux voies dans la survie des cellules du cancer colo-rectal et l’impact de leur inhibition sur le devenir cellulaire et l’évolution tumorale. L’étude a été menée sur deux lignées cellulaires provenant du même patient : SW480 (tumeur primaire) et SW620 (invasion ganglionnaire), aussi utilisées pour la réalisation de greffes sous cutanées sur le modèle murin Nude. De plus, la présence de principales protéines des NTs (TrkB) et de l’autophagie (LC3) a été analysée dans les tissus de patients. Des travaux précédents menés sur des cultures de CCR ont montré que la surexpression de TrkB était associée à la survie cellulaire. Nous avons donc choisi d’inhiber la voie des NTs avec le K252a (100nM). Sur culture cellulaire de CCR, in vitro, l’inactivation de la voie PI3K / AKT, induit une activation de l’autophagie. A l’opposé, le blocage du flux autophagique par une approche pharmacologique (avec la chloroquine, CQ ; 25µM) ou par une approche transcriptomique (siRNA anti-ATG5) induit une suractivation de la signalisation des NTs, via le couple TrkB/BDNF. Ainsi, les deux voies de survie se compensent mutuellement et la double inhibition permet l’amélioration de l’effet des simples traitements. L’utilisation des deux inhibiteurs in vivo induit une réduction spectaculaire du volume tumoral (voire même la disparition dans certains cas). Finalement, la présence de la forme active du TrkB (phospho TrkB) et de la forme active de la LC3 (LC3II), démontrant l’activation de ces deux voies dans les tissus de patients, a été observée. L’ensemble de ces résultats montre que l’activation des voies des NTs et de l’autophagie contribue à la survie des cellules de CCR. L’approche qui consiste à la double inhibition des NTs et de l’autophagie pourrait être un point majeur pour le développement de nouvelles thérapies dans le CCR
Colorectal cancer (CRC) is the first digestive cancer in occidental countries. Despite effective therapies, cases of resistance and/or recurrence exist. Our laboratory works on two signaling pathways regulating balance between survival and cell death: neurotrophins (NTs, growth factors involved in cancer cells survival) and autophagy (cellular recycling involved in stress resistance). The aim of this study was to investigate relationship between these two pathways and the impact of their inhibition on cell fate and tumor evolution.Studies were performed on two CRC cell lines derived from the same patient: SW480 (primary tumor) and SW620 (node invasion), also used for subcutaneous xenografts on Nude mouse model. In addition, presence of major proteins of NTs (TrkB) and autophagy (LC3) were assessed in patient’s tissues.Previous work showed that TrkB overexpression is associated with pro-survival signaling in CRC cell. So, we choose to inhibit NTs pathway with K252a (100 nM). As expected, inactivation of the PI3K / AKT pathway was observed and CRC cells were able to activate autophagy. At the opposite, blocking autophagic flux by pharmacologic approach (chloroquine; CQ; 25µM) or by transcriptomic approach (siRNA against ATG5) induced over-activation of the NTs pathway, via TrkB/BDNF. Thus, both survival pathways compensate each other. Moreover, dual inhibition allowed improving the effect of single treatment through a significant reduction of metabolic activity. The using of both inhibitors in vivo induces a spectacular reduction of tumor volume (or even disappearance in some cases). Presence of active form of TrkB (phospho TrkB) and active form of LC3 (LC3-II) demonstrating activation of these two pathways, in patient’s tissues have been observed. Taken together, our results showed that activation of NTs and autophagy contribute to CRC cell survival. The approach consisting of dual inhibition of NTs and autophagy could be a major point for new CRC therapies development
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Books on the topic "Neurotrophins"

1

Mocchetti, Italo. Neurobiology of the neurotrophins. Johnson City, TN: FP Graham Pub., 2001.

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Adams, Terri. Stable gradients of neurotrophins for guided neurite outgrowth. Ottawa: National Library of Canada, 2002.

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Rush, Robert A. Neurotrophin Protocols. New Jersey: Humana Press, 2000. http://dx.doi.org/10.1385/1592590608.

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Patrick, Aebischer, and Hefti Franz, eds. Neurotrophic factors. Berlin: Springer, 1999.

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Boulton, Alan A., Glen B. Baker, and Franz Hefti. Neurotrophic Factors. New Jersey: Humana Press, 1993. http://dx.doi.org/10.1385/0896032493.

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Skaper, Stephen D., ed. Neurotrophic Factors. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-536-7.

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Hefti, Franz, ed. Neurotrophic Factors. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59920-0.

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Lewin, Gary R., and Bruce D. Carter, eds. Neurotrophic Factors. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-45106-5.

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Skaper, Stephen D., ed. Neurotrophic Factors. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7571-6.

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Van de Water, Thomas R. and Koszer Samuel, eds. Clinical applications of neurotrophic factors. Philadelphia: Lippincott-Raven, 1997.

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Book chapters on the topic "Neurotrophins"

1

Dechant, Georg, and Harald Neumann. "Neurotrophins." In Advances in Experimental Medicine and Biology, 303–34. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0123-7_11.

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Nakagawara, Akira. "Neurotrophins." In Encyclopedia of Cancer, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_4051-2.

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Nakagawara, Akira. "Neurotrophins." In Encyclopedia of Cancer, 3083–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_4051.

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Nakagawara, Akira. "Neurotrophins." In Encyclopedia of Cancer, 2505–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_4051.

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Clausen, Torben, José Luis Trejo, Mark P. Mattson, Alexis M. Stranahan, Joanna Erion, Rosa Maria Bruno, Stefano Taddei, and Melinda M. Manore. "Neurotrophins." In Encyclopedia of Exercise Medicine in Health and Disease, 642–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_281.

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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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Dai, Ru-Ping, and Xin-Fu Zhou. "Neurotrophins and Pain." In Handbook of Neurotoxicity, 1805–23. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-5836-4_30.

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Hock, Christoph, K. Heese, G. Olivieri, Ch Hulette, C. Rosenberg, R. M. Nitsch, and U. Otten. "Alterations in neurotrophins and neurotrophin receptors in Alzheimer’s disease." In Advances in Dementia Research, 171–74. Vienna: Springer Vienna, 2000. http://dx.doi.org/10.1007/978-3-7091-6781-6_19.

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Castrén, E. "Neurotrophins and Psychiatric Disorders." In Neurotrophic Factors, 461–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-45106-5_17.

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West, A. E., P. Pruunsild, and T. Timmusk. "Neurotrophins: Transcription and Translation." In Neurotrophic Factors, 67–100. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-45106-5_4.

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Conference papers on the topic "Neurotrophins"

1

Dagnell, Charlotta, Johan Grunewald, Marija Kramar, Helga Haugom-Olsen, Göran Elmberger, Anders Eklund, and Caroline Olgart Hoglund. "Neurotrophins And Neurotrophin Receptors In Pulmonary Sarcoidosis - Granulomas As A Source Of Expression." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5704.

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Meuchel, Lucas W., Elizabeth A. Townsend, Michael A. Thompson, Stephen D. Cassivi, and Y. S. Prakash. "Neurotrophins Produce Nitric Oxide In Human Airway Epithelium." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5550.

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Schleputz, Marco, Marc Bernau, Michael P. Pieper, Stefan Uhlig, and Christian Martin. "Neuromodulatory Effects Of Lipopolysaccharide And Neurotrophins In Precision-Cut Lung Slices." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4166.

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Meuchel, Lucas W., Michael A. Thompson, Syed I. Zaidi, Gary C. Sieck, Richard J. Martin, and Y. S. Prakash. "Neurotrophins In Hyperoxia-Induced Enhancement Of Airway Smooth Muscle [Ca2+]i." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5307.

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"The effects of exercise on different types of neurotrophins and brain function." In International Conference on Medicine, Public Health and Biological Sciences. CASRP Publishing Company, Ltd. Uk, 2016. http://dx.doi.org/10.18869/mphbs.2016.175.

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Rezaee, F., SL Rellick, SM Akers, HA O'Leary, G. Piedimonte, and LF Gibson. "Neurotrophins Regulate Bone Marrow Stromal Cell IL-6 Expression through the MAPK Pathway." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2860.

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Scuri, Mario, Lennie Samsell, Cheryl Walton, Catherine Pitman, and Giovanni Piedimonte. "Maternal High Fat Diet Causes Down-Regulation Of Lung Neurotrophins In Rat Offspring." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1899.

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Dagnell, C., M. Mikko, M. Lofdahl, E. Roos-Engstrand, A. Blomberg, CM Skold, and C. Olgart Hoglund. "Decreased Levels of Neurotrophins in the Airways of Asymptomatic Smokers and Patients with COPD." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2954.

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Lindhout, Ivan, and Andis Klegeris. "Neurotrophins as intercellular signaling molecules of the brain regulate select immune functions of microglia." In Cell-to-Cell Metabolic Cross-Talk in Physiology and Pathology. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/cells2020-08927.

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Schulze, J., H. Staecker, T. Lenarz, D. Wedekind, D. Werner, and A. Warnecke. "The two froms of neurotrophins and their neuroprotective effect on inner ear specific cells." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1686503.

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Reports on the topic "Neurotrophins"

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Catlin, Kristen M. Role of Cytokines and Neurotrophins in the Central Nervous System in Venezuelan Equine Encephalitis Pathogenesis. Fort Belvoir, VA: Defense Technical Information Center, February 2001. http://dx.doi.org/10.21236/ad1012369.

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Shi, Yachen, Di Luan, Ruize Song, and Zhijun Zhang. The value of peripheral neurotrophins for diagnosis and antidepressant treatment response in depression: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2020. http://dx.doi.org/10.37766/inplasy2020.8.0077.

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Bambrick, Linda L. Neurotrophin Therapy of Neurodegenerative Disorders with Mitochondrial Dysfunction. Fort Belvoir, VA: Defense Technical Information Center, September 2007. http://dx.doi.org/10.21236/ada484192.

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Bambrick, Linda L. Neurotrophin Therapy of Neurodegenerative Disorders with Mitochondrial Dysfunction. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada434706.

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Yurek, David N. Neurotrophic Response to CNS Degeneration or Injury: Effects of Aging. Fort Belvoir, VA: Defense Technical Information Center, October 2004. http://dx.doi.org/10.21236/ada428519.

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Yurek, David M., and Kim B. Seroogy. Neurotrophic Response to CNS Degeneration or Injury: Effects of Aging. Fort Belvoir, VA: Defense Technical Information Center, October 2005. http://dx.doi.org/10.21236/ada463998.

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Hicks, Ramona R. Brain-Derived Neurotrophic Factor (BDNF) and Traumatic Brain Injury (Head and Spinal). Fort Belvoir, VA: Defense Technical Information Center, January 2000. http://dx.doi.org/10.21236/ada375796.

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Kuffler, Damien. Characterization of Neurotrophic & Neurotropic Interactions Between Neurons & their Muscle & Nerve Targets. Fort Belvoir, VA: Defense Technical Information Center, February 1994. http://dx.doi.org/10.21236/ada281846.

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Wishart, Heather. Imaging Effects of Neurotrophic Factor Genes on Brain Plasticity and Repair in Multiple Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada567484.

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Kuffler, Damien. Characterization of Neurotrophic and Neurotropic Interactions Between Neurons and their Muscle and Nerve Targets. Fort Belvoir, VA: Defense Technical Information Center, August 1998. http://dx.doi.org/10.21236/ada357981.

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