Relevant bibliographies by topics / Dendrite degeneration

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Dendrite degeneration'

Author: Grafiati
Published: 4 June 2021
Last updated: 3 February 2022

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Journal articles on the topic "Dendrite degeneration"

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Lin, Chin-Hsien, Hsun Li, Yi-Nan Lee, Ying-Ju Cheng, Ruey-Meei Wu, and Cheng-Ting Chien. "Lrrk regulates the dynamic profile of dendritic Golgi outposts through the golgin Lava lamp." Journal of Cell Biology 210, no. 3 (July 27, 2015): 471–83. http://dx.doi.org/10.1083/jcb.201411033.

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Constructing the dendritic arbor of neurons requires dynamic movements of Golgi outposts (GOPs), the prominent component in the dendritic secretory pathway. GOPs move toward dendritic ends (anterograde) or cell bodies (retrograde), whereas most of them remain stationary. Here, we show that Leucine-rich repeat kinase (Lrrk), the Drosophila melanogaster homologue of Parkinson’s disease–associated Lrrk2, regulates GOP dynamics in dendrites. Lrrk localized at stationary GOPs in dendrites and suppressed GOP movement. In Lrrk loss-of-function mutants, anterograde movement of GOPs was enhanced, whereas Lrrk overexpression increased the pool size of stationary GOPs. Lrrk interacted with the golgin Lava lamp and inhibited the interaction between Lva and dynein heavy chain, thus disrupting the recruitment of dynein to Golgi membranes. Whereas overexpression of kinase-dead Lrrk caused dominant-negative effects on GOP dynamics, overexpression of the human LRRK2 mutant G2019S with augmented kinase activity promoted retrograde movement. Our study reveals a pathogenic pathway for LRRK2 mutations causing dendrite degeneration.
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Yang, Wei-Kang, and Cheng-Ting Chien. "Beyond being innervated: the epidermis actively shapes sensory dendritic patterning." Open Biology 9, no. 3 (March 2019): 180257. http://dx.doi.org/10.1098/rsob.180257.

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Sensing environmental cues requires well-built neuronal circuits linked to the body surface. Sensory neurons generate dendrites to innervate surface epithelium, thereby making it the largest sensory organ in the body. Previous studies have illustrated that neuronal type, physiological function and branching patterns are determined by intrinsic factors. Perhaps for effective sensation or protection, sensory dendrites bind to or are surrounded by the substrate epidermis. Recent studies have shed light on the mechanisms by which dendrites interact with their substrates. These interactions suggest that substrates can regulate dendrite guidance, arborization and degeneration. In this review, we focus on recent studies of Drosophila and Caenorhabditis elegans that demonstrate how epidermal cells can regulate dendrites in several aspects.
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Bauer, Carol A., Thomas J. Brozoski, and Kristin Myers. "Primary afferent dendrite degeneration as a cause of tinnitus." Journal of Neuroscience Research 85, no. 7 (2007): 1489–98. http://dx.doi.org/10.1002/jnr.21259.

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TRIBBLE, JAMES R., STEPHEN D. CROSS, PAULINA A. SAMSEL, FRANK SENGPIEL, and JAMES E. MORGAN. "A novel system for the classification of diseased retinal ganglion cells." Visual Neuroscience 31, no. 6 (November 2014): 373–80. http://dx.doi.org/10.1017/s0952523814000248.

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AbstractRetinal ganglion cell (RGC) dendritic atrophy is an early feature of many forms of retinal degeneration, providing a challenge to RGC classification. The characterization of these changes is complicated by the possibility that selective labeling of any particular class can confound the estimation of dendritic remodeling. To address this issue we have developed a novel, robust, and quantitative RGC classification based on proximal dendritic features which are resistant to early degeneration. RGCs were labeled through the ballistic delivery of DiO and DiI coated tungsten particles to whole retinal explants of 20 adult Brown Norway rats. RGCs were grouped according to the Sun classification system. A comprehensive set of primary and secondary dendrite features were quantified and a new classification model derived using principal component (PCA) and discriminant analyses, to estimate the likelihood that a cell belonged to any given class. One-hundred and thirty one imaged RGCs were analyzed; according to the Sun classification, 24% (n = 31) were RGCA, 29% (n = 38) RGCB, 32% (n = 42) RGCC, and 15% (n = 20) RGCD. PCA gave a 3 component solution, separating RGCs based on descriptors of soma size and primary dendrite thickness, proximal dendritic field size and dendritic tree asymmetry. The new variables correctly classified 73.3% (n = 74) of RGCs from a training sample and 63.3% (n = 19) from a hold out sample indicating an effective model. Soma and proximal dendritic tree morphological features provide a useful surrogate measurement for the classification of RGCs in disease. While a definitive classification is not possible in every case, the technique provides a useful safeguard against sample bias where the normal criteria for cell classification may not be reliable.
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Chopra, Ravi, David D. Bushart, and Vikram G. Shakkottai. "Dendritic potassium channel dysfunction may contribute to dendrite degeneration in spinocerebellar ataxia type 1." PLOS ONE 13, no. 5 (May 30, 2018): e0198040. http://dx.doi.org/10.1371/journal.pone.0198040.

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Koike, Tatsuro, Yi Yang, Kazuhiko Suzuki, and Xiaoxiang Zheng. "Axon & dendrite degeneration: Its mechanisms and protective experimental paradigms." Neurochemistry International 52, no. 4-5 (March 2008): 751–60. http://dx.doi.org/10.1016/j.neuint.2007.09.007.

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Azizah, Nurul, Sisca Sisca, and Rasiha Rasiha. "REGENERASI DENDRIT SEL GANGLION RETINA: PERAN INSULIN UNTUK MENGEMBALIKAN PENGLIHATAN PADA GLAUKOMA." Al-Iqra Medical Journal : Jurnal Berkala Ilmiah Kedokteran 1, no. 2 (November 12, 2019): 74–83. http://dx.doi.org/10.26618/aimj.v1i2.2758.

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Glaukoma is a leading cause of irreversible blindness worldwide. This disease is associated with characteristic damage to the optic nerve and permanent retinal ganglion cell (RGC) degeneration. A crucial step towards circuit repair in glaucoma is to promote damaged RGCs to regenerate not only axons, but also dendrites to successfully reconnect with their synaptic partners. The latest research showed that insulin signalling has the capacity to regenerate dendrites dan injured synapses, therefore the use of insulin raises a new paradigm as a new pro-regenerative therapeutic target for the disease of glaucoma. This literature review is made using literature searching of valid journals with inclusion and exclusion criteria. On the experiment of insulin’s effectivity, it is valued using 4 indicators; promote dendrite regeneration, restore synaptic density, rescue retinal function, robust neuronal survival. Based on in vivo experiment, insulin endowed with the ability to effectively restore dendritic morphology thus enhancing the function and survival of RGC through mTORC1 (mammalian target of rapamycin complex 1) and mTORC2 (mammalian target of rapamycin complex 2) signalling, this supports that that it can be promising therapeutic targets to counter progressive RGC neurodegeneration and vision loss in glaucoma.
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Satoh, Daisuke, Ritsuko Suyama, Ken‐ichi Kimura, and Tadashi Uemura. "High‐resolution in vivo imaging of regenerating dendrites of D rosophila sensory neurons during metamorphosis: local filopodial degeneration and heterotypic dendrite–dendrite contacts." Genes to Cells 17, no. 12 (November 15, 2012): 939–51. http://dx.doi.org/10.1111/gtc.12008.

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Plowey, Edward D., Jon W. Johnson, Erin Steer, Wan Zhu, David A. Eisenberg, Natalie M. Valentino, Yong-Jian Liu, and Charleen T. Chu. "Mutant LRRK2 enhances glutamatergic synapse activity and evokes excitotoxic dendrite degeneration." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1842, no. 9 (September 2014): 1596–603. http://dx.doi.org/10.1016/j.bbadis.2014.05.016.

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Kolotov, K. A., and P. G. Rasputin. "MONOCYTIC CHEMOTACTIC PROTEIN-1 IN PHYSIOLOGY AND MEDICINE (REVIEW OF LITERATURE)." Perm Medical Journal 35, no. 3 (December 15, 2018): 99–105. http://dx.doi.org/10.17816/pmj35399-105.

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Monocytic chemotactic protein-1-cytokin, attributed to the group of chemokins, is the most powerful factor of monocyte chemotaxis in the body of mammalians as well as memory T-cells and dendrite cells to inflammatory foci and is produced upon tissue damages or infection introduced. MCP-1 is mainly secreted by monocytes, macrophages and dendrite cells. Clinical significance of MCP-1 consists in participation of some diseases in pathogenesis: psoriasis, rheumatoid arthritis, atherosclerosis. MCP-1 is involved into the processes of developing central nervous system diseases, which are characterized by neuronal degeneration. Besides, this cytokine plays a significant role in vascular complications of type 2 diabetes mellitus and formation of obesity insulin resistance.
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Dissertations / Theses on the topic "Dendrite degeneration"

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Rooney, Timothy M. "Genes Required for Wallerian Degeneration Also Govern Dendrite Degeneration: A Dissertation." eScholarship@UMMS, 2004. http://escholarship.umassmed.edu/gsbs_diss/775.

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Neurons comprise the main information processing cells of the nervous system. To integrate and transmit information, neurons elaborate dendritic structures to receive input and axons to relay that information to other cells. Due to their intricate structures, dendrites and axons are susceptible to damage whether by physical means or via disease mechanisms. Studying responses to axon injury, called Wallerian degeneration, in the neuronal processes of Drosophila melanogaster has allowed the identification of genes that are required for injury responses. Screens in Drosophila have identified dsarm and highwire as two genes required for axon degeneration; when these genes are mutated axons fail to degenerate after injury, even when completely cut off from the neuronal cell body. We found that these genes are also required for dendrite degeneration after injury in vivo. Further, we reveal differences between axon and dendrite injury responses using in vivo timelapse recordings and GCaMP indicators of intracellular and mitochondrial calcium transients. These data provide insights into the neuronal responses to injury, and better define novel targets for the treatment of neurodegenerative diseases.
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Rooney, Timothy M. "Genes Required for Wallerian Degeneration Also Govern Dendrite Degeneration: A Dissertation." eScholarship@UMMS, 2015. https://escholarship.umassmed.edu/gsbs_diss/775.

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Neurons comprise the main information processing cells of the nervous system. To integrate and transmit information, neurons elaborate dendritic structures to receive input and axons to relay that information to other cells. Due to their intricate structures, dendrites and axons are susceptible to damage whether by physical means or via disease mechanisms. Studying responses to axon injury, called Wallerian degeneration, in the neuronal processes of Drosophila melanogaster has allowed the identification of genes that are required for injury responses. Screens in Drosophila have identified dsarm and highwire as two genes required for axon degeneration; when these genes are mutated axons fail to degenerate after injury, even when completely cut off from the neuronal cell body. We found that these genes are also required for dendrite degeneration after injury in vivo. Further, we reveal differences between axon and dendrite injury responses using in vivo timelapse recordings and GCaMP indicators of intracellular and mitochondrial calcium transients. These data provide insights into the neuronal responses to injury, and better define novel targets for the treatment of neurodegenerative diseases.
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Ha, Andrew. "Drosophila Hook-Related Protein (Girdin) is Essential for Sensory Dendrite Maintenance." University of Toledo / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1430408605.

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Shi, Ri Yi. "Neuronal Survival After Dendrite Amputation: Investigation of Injury Current Blockage." Thesis, University of North Texas, 1988. https://digital.library.unt.edu/ark:/67531/metadc501278/.

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After dendrite transection, two primary injury current pathways may acount for cell death: (1) the lesion current at the site of injury and (2) the voltage sensitive calcium channels along the dendrite. Lesions were made with a laser microbeam in mouse spinal monolayer cell cultures. Polylysine was tried as a positively charged "molecular bandage" to block the lesion current. The calcium channel blockers, verapamil and nifedipine, were used to reduce the calcium channel current. Control toxicity curves were obtained for all three compounds. The results show that neither verapamil, nifedipine, nor polylysine (MW: 3,300) protect nerve cells after dendrite amputation 100 ptm from the soma. The data also indicate that these compounds do not slow the process of cell death after such physical trauma.
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Park, Katya. "Molecular Mechanisms Regulating Neurite Growth, Innervation and Survival." Thesis, 2010. http://hdl.handle.net/1807/26513.

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The establishment of correct neural circuitry in the nervous system requires the interplay, integration, and coordination of a diverse set of cells and signals during development and in the adult. Two important events are the regulated initiation and growth of dendrites that receive and process synaptic information, and the establishment and maintenance of appropriate neural connectivity. The goals of this study are to identify the molecular mechanisms underlying dendrite growth and initiation, and to understand how neural connectivity is maintained in the adult nervous system. I first identified a novel intracellular signal transduction pathway involving two kinases important in regulating dendrite development. I showed that the ILK-GSK3beta pathway is required for dendrite growth and initiation in both peripheral and central nervous system neurons. I then asked how neural connectivity is maintained in the adult nervous system by examining the role of myelin in the intact nervous system. My results indicate that when myelin contacts aberrantly growing axons, it activates on those axons the p75 neurotrophin receptor (p75NTR), which in turn causes the local degeneration of those axons. I further identified the signal transduction pathway required for axon degeneration consisting of p75NTR and intracellular signaling proteins activated by this receptor, Rho-GDI, Rho, and caspase 6. This data establishes p75NTR as an important regulator of neural connectivity and identifies for the first time a degeneration-inducing signal transduction pathway activated by myelin. It also provides an explanation for why myelin inhibits regeneration of injured central nervous system axons. Taken together, I identified a new signaling pathway important for regulating dendrite initiation and growth, and a novel role for myelin in maintaining neural connectivity. Both of these findings contribute to our knowledge of how such connectivity is established during development and maintained in the adult nervous system.
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Boyle, Lia. "A Precision Medicine Approach to Understanding KIF1A Associated Neurological Disorder." Thesis, 2021. https://doi.org/10.7916/d8-0nef-s787.

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The functional compartmentalization underlying neuronal polarity makes tightly regulated intracellular transport between the cell body, axons, and dendrites essential for proper development and homeostatic maintenance. Disruptions to neuronal trafficking are a major cause of neurodegenerative disease. Pathogenic variants in the microtubule motor protein KIF1A cause KIF1A Associated Neurological Disorder (KAND), a spectrum of rare neurodegenerative conditions. KAND is clinically and genetically heterogeneous, with a broad phenotypic spectrum and over a hundred pathogenic variants identified. KAND is poorly understood at both the clinical and molecular level, and there is currently no treatment. This work characterizes the natural history of KAND and describes a novel heuristic severity score. This severity score is then used to show how the location of pathogenic missense variants within the KIF1A motor domain correlates with disease severity, providing evidence the clinical phenotypic heterogeneity in KAND reflects and parallels the molecular phenotypes. Insights from the neuropathology of deceased KAND patients is used to focus a histopathologic assessment of the C3-Kif1aLgdg mouse model. C3-Kif1aLgdg/Lgdg mice have a cerebellar axonal torpedo phenotype, paralleling some of the pathological changes seen in the patients. Phenotypically, the C3-Kif1aLgdg mice were found to recapitulate some of the symptoms seen in patients including progressive spasticity and gait abnormalities associated with hind limb paralysis. To model the disease at a cellular level, iPSCs were derived from affected individuals and successfully used to generate neural stem cells and neurons. These patient-derived neurons were found to have increased markers of protein aggregates, a cellular phenotype that can be used to test potential treatments. Taken together, these studies provide foundational knowledge for future therapeutic development.
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Book chapters on the topic "Dendrite degeneration"

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Santina, Luca Della, and Yvonne Ou. "Dendrite Degeneration in Glaucoma." In Dendrites, 581–97. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56050-0_22.

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Lee, Sebum, Yulei Shang, and Eric J. Huang. "Mechanisms of Dendrite Degeneration in Amyotrophic Lateral Sclerosis." In Dendrites, 545–79. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56050-0_21.

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Altrup, U., A. Lücke, A. Lehmenkühler, and E. J. Speckmann. "Sprouting and Degeneration of Dendrites of the Identified Neuron B3 in the Buccal Ganglia of Helix Pomatia after Epileptic Activity." In Physiology, Pharmacology and Development of Epileptogenic Phenomena, 61–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-46732-5_14.

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Wang, Fan, Jing Yang, and Zhigang He. "Axon maintenance and degeneration." In Cellular Migration and Formation of Axons and Dendrites, 217–30. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-814407-7.00010-9.

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Conference papers on the topic "Dendrite degeneration"

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Costa, Luisy Karen Lemos, Caio Marques Da Silva, Bárbara Monique De Freitas Vasconcelo, Fernanda Fonsêca Monteiro Freire, and Juliana Minervina De Souza Freire. "ALZHEIMER E SUAS BASES FISIOPATOLÓGICAS." In II Congresso Brasileiro de Saúde On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1505.

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Introdução: A doença do Alzheimer (DA) é uma doença neurodegenerativa crônica, na qual causa deterioração cognitiva de forma progressiva. O processo fisiopatológico e os sintomas são ocasionados em virtude da morte das células nervosas e perda de tecido em todo o cérebro, isso se dá devido ao mal funcionamento das proteínas Beta-amiloide e Tau. Objetivos: Compreender a fisiopatologia associada a doença de Alzheimer. Material e métodos: Foi realizada uma revisão de literatura integrativa usando os bancos de dados Revista Brasileira de Neurologia e Scielo, aplicando os descritores “Doença de Alzheimer”; “Fisiopatologia Alzheimer” e “Sinais e sintomas do Alzheimer”. Usou-se como critério de inclusão os artigos em inglês e português que estivessem no período entre os anos de 2015 a 2021. Resultados: O acúmulo das proteínas Beta-amiloide e Tau, forma placas e emaranhados em regiões específicas do cérebro que inibem as sinapses neuronais necessárias para o funcionamento do sistema nervoso central. A localização dessas proteínas, determinam os sinais e sintomas da Doença de Alzheimer, ocasionando lesões permanentes a nível celular, como a degeneração neurofibrilar que condiz ao espessamento e tortuosidade nas células neurofibrilas localizadas no pericário neuronal, podendo alterar os constituintes celulares gerais. As proteínas beta-amiloide estão relacionadas no auxílio do sistema imunológico nervoso central, que atuam na captura de microrganismos que passagem pela barreira hematoencefálica, a forma deficiente desta proteína ocasiona inúmeras alterações nas células nervosas, principalmente a destruição dos dendritos que são as projeções comunicantes nos neurônios. Em células nervosas saudáveis, a proteína tau contribui na formação e estabilização dos microtúbulos, os quais são fundamentais para a comunicação entre os neurônios. Nos pacientes com a doença de Alzheimer a proteína tau para de funcionar corretamente, pois separa-se dos microtúbulos e criam formas desorganizadas que irão obstruir os microtúbulos. Conclusão: Diante das inibições de sinapses neuronais, as células cerebrais se degeneram e morrem, gerando perda de memória e algumas funções mentais. Além de ser uma doença degenerativa tão invasiva, é necessário promover uma melhor qualidade de vida para os pacientes, um esforço conjunto entre a família e os profissionais da saúde, como fisioterapeuta, fonoaudiólogo, psicólogo, nutricionista, terapeuta ocupacional, entre outros.
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