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Relevant bibliographies by topics / Astrocytes Neuroinflammation / Dissertations / Theses

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Dissertations / Theses on the topic 'Astrocytes Neuroinflammation'

Author: Grafiati

Published: 10 December 2022

Last updated: 19 July 2025

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1

Brothers, Holly M. "Neuroinflammation, Glutamate Regulation and Memory." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1363603410.

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Wu, Celina. "Dual agonist-antagonist functions of FTY720 influence neuroinflammation-relevant responses in human astrocytes." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=110720.

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Astrocytes are the most abundant glia in the central nervous system (CNS), classically identified by their high expression of the intermediate filament, glial fibrillary acidic protein (GFAP). Astrocytes participate in a number of biochemical events important for CNS functions and play a dynamic role in regulating CNS injury/repair processes. In chronic inflammatory conditions such as multiple sclerosis (MS), astrocytes undergo pathophysiological changes that lead to a feature termed astrogliosis (Liberto, Albrecht et al. 2004; Sidoryk-Wegrzynowicz, Wegrzynowicz et al. 2011). Astrogliosis is c

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3

Hoskins, Andrew. "The Role of IRF1 in the Brain and in Adaptive Responses of Astrocytes." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5757.

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In neurodegenerative diseases, the CNS becomes inflamed through activation of pathways, including the NF-B pathway. Some of the therapies for those diseases target neuroinflammatory pathways. Here, we explore the mechanisms for the upregulation of a subset of genes following a restimulation of the NF-B pathway. We discover that this upregulation occurs independent of IRF1 expression and type 1 interferon signaling. A knockdown of IRF1 using siRNA and an inhibition of JAK proteins using inhibitor AG490 both had no effect on priming. A secreted factor was found to upregulate the expression of bo

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4

Clement, Tifenn. "Contribution of astrocytes in brain vulnerability after juvenile mild traumatic brain injury." Thesis, Bordeaux, 2020. http://www.theses.fr/2020BORD0141.

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Les astrocytes sont des cellules cruciales pour une variété de fonctions physiologiques cérébrales telles que l’homéostasie, le métabolisme, le couplage neurovasculaire ou la régulation de la neurotransmission. Lors de lésions cérébrales, les astrocytes deviennent réactifs et tiennent un rôle prépondérant dans la réponse neuroinflammatoire. Cette réactivité astrocytaire est hétérogène et dépend de nombreux paramètres tels que le type et la sévérité de la lésion, la proximité de l’astrocyte à la lésion, ou encore l’état de maturité du cerveau. Cependant, la réponse spécifique des astrocytes au

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5

Phillips, Emma Claire. "Investigating the contribution of astrocytes and neuroinflammation to pathological tau changes in Alzheimer's disease." Thesis, King's College London (University of London), 2017. https://kclpure.kcl.ac.uk/portal/en/theses/investigating-the-contribution-of-astrocytes-and-neuroinflammation-to-pathological-tau-changes-in-alzheimers-disease(d96f6fa6-6870-4461-82b2-0a19d5507eab).html.

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Alzheimer’s disease (AD) is a progressive neurodegenerative disease characterised by accumulation of ß-amyloid in extracellular plaques, intracellular neurofibrillary tangles composed of abnormally phosphorylated and aggregated tau, and widespread synaptic dysfunction and neuron loss that underlie the clinical symptoms of AD. Glial activation and a neuroinflammatory immune response is also a key aspect of the pathological progression of AD. The activation of astrocytes appears to be particularly associated with pathological changes in tau. This thesis aims to investigate the association betwee

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Domiziana, De Tommaso. "Astrocytes contribute to neuroinflammation during EAE by shaping the CNS microenvironment via Rai signalling." Doctoral thesis, Università di Siena, 2020. http://hdl.handle.net/11365/1105117.

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Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS). One of the pathological hallmarks of MS is the T cells-mediated destruction of myelin sheath, which result in axonal damage and subsequent neurological dysfunction. Current MS therapies are focused on immunosuppression as they are aimed at limiting the entry of immune cells into CNS, thereby preventing neuroinflammation. Although these therapies have been shown to be potent disease-modifying agents they fail to prevent or reverse disease progression. Astrocytes, among CNS resident cells, has been recently sug

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7

Dorey, Evan J. "Apolipoprotein E Isoforms Differentially Regulate Amyloid-β Stimulated Inflammation in Rat and Mouse Astrocytes". Thesis, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/23581.

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Neuroinflammation occurs in Alzheimer’s disease (AD) brain, and plays a role in neurodegeneration. The main aim of this study was to determine how treatments with exogenous apolipoprotein E (ApoE2, E3 and E4 isoforms), a genetic risk factor for AD, affects the amyloid-β (Aβ) induced inflammatory response in vitro in astrocytes. Recombinant, lipid-free ApoE4 was found not to affect Aβ-induced inflammation in rat astrocytes, while ApoE2 showed a protective effect. Mouse cells expressing human ApoE isoforms, which have similar lipidation and modification to native human ApoE, showed ApoE4 promoti

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8

Hsu, Meng-Ping. "Mechanisms Underlying Specificity in the Biology of the IL-6/gp130 Cytokines in Astrocytes and Microglia." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/18014.

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The gp130 family of cytokines includes IL-6, OSM, LIF, IL-11, CNTF, CLC/CLF-1 and CT-1. Members of this family are structurally similar and bind to at least one subunit of gp130 in their receptor complexes. Furthermore, they activate common signal transduction pathways, including the JAK/STAT and SHP2 pathways. However, despite these common features, cytokine-specific functions are known to exist. Two types of glial cells, astrocytes and microglia, are involved in the host response against CNS insults and release a variety of inflammatory cytokines and chemokines, including gp130 cytokines. Ho

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9

Ceyzériat, Kelly. "Modulation de la réactivité astrocytaire par ciblage de la voie JAK2-STAT3 : conséquences dans des modèles murins de la maladie d’Alzheimer." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS556/document.

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Les astrocytes sont des éléments clés de la physiologie cérébrale. Dans les maladies neurodégénératives comme la maladie d’Alzheimer (MA), les astrocytes deviennent réactifs. Cette réactivité astrocytaire (RA) est essentiellement caractérisée par des changements morphologiques. En revanche, les effets de la réactivité sur les fonctions de support des astrocytes sont mal connus. De plus, les cascades de signalisation qui conduisent à la RA restent à déterminer. Les objectifs de ce projet étaient de : 1/ démontrer que la voie JAK2-STAT3 (Janus Kinase 2 - Signal Transducer and Activator of Transc

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10

Frakes, Ashley E. "The Role of Neuroinflammation in the Pathogenesis of Amyotrophic Lateral Sclerosis." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1417649954.

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11

Guillot, Flora. "Caractérisation de l'infiltrat lymphocytaire et de la réactivité astrocytaire dans un modèle de neuroinflammation autoimmune." Nantes, 2014. https://archive.bu.univ-nantes.fr/pollux/show/show?id=eba4b03e-07fe-4198-a88d-16cbb5f7f5eb.

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La sclérose en plaques (SEP) est une maladie autoimmune, démyélinisante et dégénérative du système nerveux central (SNC). La réponse T CD4 est impliquée dans le développement de la SEP et son modèle animal : l'encéphalomyélite autoimmune expérimentale (EAE). De récentes données montrent que les lymphocytes T CD8 anti-myéline peuvent être impliqués d'autant plus qu'ils sont présents abondamment dans les lésions SEP. Afin de mieux comprendre la contribution des T CD8 pathogéniques, deux récents modèles ont été évalués. Le premier consiste à immuniser des souris avec un épitope de la myéline T CD

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12

Filipello, F. "MOLECULAR AND CELLULAR MECHANISMS IN ASTROCYTE-T CELL CROSS-TALK." Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/232403.

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Migration of encephalitogenic T cells into the brain parenchima through the blood–brain barrier (BBB) is a crucial feature for initiating tissue injury in different neuroinflammatory diseases. The BBB is comprised of astrocyte processes and endothelial cells, which form the lumen of the brain microvasculature and help in maintaining immune quiescence through contact-dependent mechanisms as well as release of soluble factors. Activated CD4+ T cells may establish physical contacts with astrocytes, thereby reciprocally influencing cellular activity and functions. In addition, astrocytes and CD4 T

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13

MADEDDU, SILVIA. "Unique gene expression profiles of microglia and astrocytes following innate immune activation." Doctoral thesis, Università degli Studi di Cagliari, 2014. http://hdl.handle.net/11584/266460.

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Both astrocytes and microglia are often activated in association with diseases of the central nervous system (CNS), including virus-induced neurological disease. Understanding how activation alters the transcriptome of these cells may offer valuable insight in regards to how activated cells mediate neurological damage. Furthermore, identifying common and unique pathways of gene expression during activation may provide new insight into the distinct roles these cells have in the CNS during infection and inflammation. In the current study, we utilized microarray analysis to examine the response o

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14

Dreux, Virginie. "Supplémentatiοn οrale en glutamine et répοnse hypοthalamique au cοurs de l'οbésité induite par l'alimentatiοn". Electronic Thesis or Diss., Normandie, 2024. http://www.theses.fr/2024NORMR065.

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L’obésité représente un enjeu majeur de santé publique. Cette maladie multifactorielle présente un dimorphisme sexuel marqué aussi bien dans sa prévalence et son évolution que dans les comorbidités associées. Elle est caractérisée par une inflammation chronique de bas grade et par un déséquilibre de l’homéostasie énergétique. Cette régulation énergétique est médiée par l’action coordonnée des neurones et des cellules gliales hypothalamiques. Néanmoins, des preuves croissantes soutiennent que la présence d’une inflammation et d’une gliose seraient responsables d’un découplage de l’unité neurogl

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15

Ben, Haim Lucile. "Modulation of the JAK2/STAT3 pathway in vivo : understanding reactive astrocyte functional features and contribution to neurodegenerative diseases." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066534/document.

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Les astrocytes deviennent réactifs dans les maladies neurodégénératives (MND) comme la maladie d’Alzheimer (MA) et de Huntington (MH) mais les conséquences fonctionnelles de cette réactivité sont peu connues. Dans cette étude, nous avons évalué 1) les voies de signalisation impliquées dans la réactivité astrocytaire, 2) la contribution des astrocyte réactifs (AR) à la dysfonction neuronale dans des modèles de MND et 3) les caractéristiques fonctionnelles des AR.Nous avons montré que la voie JAK2/STAT3 est responsable de la réactivité astrocytaire dans des modèles murins de la MA et la MH. Nous

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16

Herber, Donna Lorraine. "Neuroinflammation in Alzheimers disease : characterization and modification of the response of transgenic mice to intrahippocampal lipopolysaccharide administration /." [Tampa, Fla.] : University of South Florida, 2004. http://purl.fcla.edu/fcla/etd/SFE0001075.

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Lhuillier, Alice. "Identification de programmes d'activation macrophagique et microgliale dans les formes progressives de la sclérose en plaques." Phd thesis, Université Claude Bernard - Lyon I, 2014. http://tel.archives-ouvertes.fr/tel-01056829.

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La sclérose en plaques (SEP) est une maladie neuro-inflammatoire chronique, première cause de handicap chez le jeune adulte. Actuellement, aucun traitement ne freine l'aggravation des symptômes liée aux formes progressives. Bien que connue, l'implication des macrophages et de la microglie dans la démyélinisation et l'atteinte axonale doit être plus finement caractérisée. Ce d'autant plus que la plasticité fonctionnelle de ces cellules suggère une réponse spécifique selon la pathologie, la localisation des lésions et le stade évolutif de la maladie. Ce travail de thèse a consisté en une caracté

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18

O'Callaghan, Paul. "Heparan Sulfate in the Amyloidosis and Inflammation of Alzheimer’s Disease." Doctoral thesis, Uppsala universitet, Geriatrik, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-159927.

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Alzheimer’s disease (AD) is a neurodegenerative disorder, with extensive evidence implicating the misfolding, aggregation and deposition of the amyloid-β (Aβ) peptide as central to the pathogenesis. Heparan sulfate (HS) is an interactive glycosaminoglycan, attached to core proteins as HS proteoglycans (HSPGs). HSPGs are present on cell surfaces and in the extracellular matrix where they facilitate multiple signaling functions, but HS is also consistently present in all amyloid deposits, including those of AD. In amyloidosis HS has been studied as an aggregation template, promoting fibril forma

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19

Jukkola, Peter I. "The Role of Potassium Ion and Water Channels in an Animal Model ofMultiple Sclerosis." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1397656579.

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20

CARTA, ELISA. "Studio dell’attività antivirale e/o anti-infiammatoria di nuove molecole di sintesi e/o di farmaci noti." Doctoral thesis, Università degli Studi di Cagliari, 2016. http://hdl.handle.net/11584/266698.

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This thesis collects the work I have done during the three-year of my PhD Course. During my first year I have started a path that has allowed me to acquire different techniques to set up and culture animal cell lines as well as to evaluate the cytotoxic and anti-picornavirus activities of a class of novel synthetic quinoxaline (Part I). Part of the second and all the third year was spent at the NIAID/NIH, Hamiltion MT, USA, in the laboratory of persistent viral diseases under the supervision of dr. Bruce Chesebro investigating the effect of statins for the control of neuroinflammation (P

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Vizuete, Adriana Fernanda Kuckartz. "Avaliação da neuroinflamação e da atividade astrocitária em modelo de epilepsia por Li-pilocarpina: S100B possível marcador e alvo farmacológico." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2017. http://hdl.handle.net/10183/165307.

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A epilepsia do lobo temporal (ELT) é a um dos casos mais frequente epilepsia em humanos e de maior refratariedade nos pacientes. A maioria dos fármacos antiepilépticos são moduladores da atividade neuronal e atuam sobre canais iônicos do receptor GABAA. Estudos vêm demonstrando o papel das células gliais e da neuroinflamação na epileptogênese e a modulação desta resposta pode ser um alvo potencial para drogas adjuvantes aos fármacos anti-epilépticos. Astrócitos são células gliais participantes da sinapse tripartite, moduladores da atividade neuronal. Os astrócitos são capazes de promover a hom

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Bernardi, Caren Luciane. "Parâmetros comportamentais e bioquímicos gliais e inflamatórios em pacientes com lesão da medula espinhal submetidos à dança, e em ratos Wistar submetidos aos protocolos de exercício voluntário e forçado." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2013. http://hdl.handle.net/10183/143581.

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Os objetivos principais desta tese foram avaliar parâmetros bioquímicos gliais, inflamatórios e comportamentais em pacientes com lesão medular (LM) submetidos a um protocolo de dança, e em ratos submetidos aos protocolos de exercício voluntário e forçado. Para tanto, foram realizados 4 experimentos. No primeiro, os ratos foram submetidos a 4 semanas de exercício moderado em esteira ergométrica (20 min por dia). No segundo, os animais foram submetidos à 4 semanas de exercício voluntário em rodas de correr (12 horas por dia). No terceiro experimento, os ratos foram expostos à esteira ergométrica

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Campos, Torres Antonio. "Contribution à l' étude des interactions neurones-glie dans la plasticité post-lésionnelle du système nerveux central adulte : la compensation vestibulaire." Paris 6, 2005. http://www.theses.fr/2005PA066484.

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Facci, Laura. "Role of microglia and astrocytes in inflammatory processes involving neurological diseases, chronic pain, and psychiatric disorders, with emphasis on the purinergic P2X7 receptor." Doctoral thesis, Università degli studi di Padova, 2013. http://hdl.handle.net/11577/3422630.

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Under pathological conditions microglia (resident central nervous system (CNS) immune cells) become activated, and produce reactive oxygen and nitrogen species and pro-inflammatory cytokines: molecules that can contribute to disorders including stroke, traumatic brain injury, progressive neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, multiple sclerosis, and several retinal diseases. Given that ATP is frequently released from CNS neurons during tissue damage and inflammation, its actions on microglia-mediated toxicity are especially

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25

Van, Gijsel-Bonnello Manuel. "Neuroinflammation et perturbations métaboliques au cours du vieillissement cérébral normal et pathologique (maladie d'Alzheimer) : exploration du potentiel protecteur de la pantéthine." Thesis, Aix-Marseille, 2015. http://www.theses.fr/2015AIXM5058/document.

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Nous avons exploré les altérations cérébrales liées à l’âge, dans des conditions physiologiques ou pathologiques (maladie d’Alzheimer), à partir de deux modèles murins, SAM-P8 (souris à sénescence accélérée) et 5xFAD..Dans les deux cas, les animaux montrent des signes de neuroinflammation avec libération de la principale cytokine pro-inflammatoire IL-1β. Ces troubles sont sans conteste d’origine endogène, puisqu’ils n’ont pas été observés chez les témoins. Il faut souligner que les astrocytes 5xFAD ont été prélevés chez des nouveau-nés et par conséquent leur état inflammatoire signifie que la

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Erta, Cañabate Maria. "Role of astrocytic IL-6 and IL-6R in normal physiology and neuroinflammation." Doctoral thesis, Universitat Autònoma de Barcelona, 2014. http://hdl.handle.net/10803/275952.

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La Interleucina 6 (IL-6) és una citocina altament multifuncional, amb moltes accions pleiotròpiques, considerada una de les principals citocines controlant el sistema immune i coordinant-lo amb els sistemes nerviós i endocrí. La IL-6 es produeix en molts tipus cel·lulars dins del sistema nerviós central (SNC) i al seu torn, múltiples cèl·lules hi poden respondre. Per tant, és necessari caracteritzar quina és la contribució específica de cada tipus cel·lular en el paper global de la IL-6, tant en condicions fisiològiques com patològiques. Com que els astròcits tenen una important resposta enfro

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Marinelli, Carla. "Toll-like receptors as transducer of inflammatory signals in glia: the astrocyte-microglia connection." Doctoral thesis, Università degli studi di Padova, 2015. http://hdl.handle.net/11577/3424616.

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In physiological conditions glia in the central nervous system (CNS) can produce and release protective factors such as anti-oxidant molecules and neurotrophic factors (Sofroniew et al., 2010). Events that impinge on CNS homeostatic balance can induce local inflammatory responses (Carson et al., 2006). Reactive glia can participate producing pro-inflammatory mediators such as chemokines, cytokines, purines and free radicals. Toll-like receptors (TLRs) are involved in injury responses of nervous system tissue and in neuropathic pain. Here we have investigated the cross-talk mechanisms between

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MARTORANA, FRANCESCA. "Mitochondria as the core of neuroinflammation and neurodegeneration in models of neuronal and astrocytic dysfunction." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2020. http://hdl.handle.net/10281/259338.

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Le malattie neurodegenerative sono caratterizzate da disfunzione e perdita di specifiche popolazioni neuronali in risposta ad invecchiamento o eventi tossici o traumatici. Tuttavia, recentemente, è diventato chiaro che la disfunzione astrocitica ha un ruolo importante nei processi degenerativi. Infatti, gli astrociti rappresentano la popolazione cellulare maggiore del Sistema Nervoso Centrale (SNC) e costituiscono l’elemento principale per la sua omeostasi. Alterazioni biochimiche e strutturali degli astrociti durante la neuroinfiammazione rappresentano una risposta fisiologica a danni a caric

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Shanaki, Bavarsad Mahsa. "Astrocyte-targeted production of IL-10 reduces the neuroinflammatory response associated to TBI and improves neurodegeneration." Doctoral thesis, Universitat Autònoma de Barcelona, 2020. http://hdl.handle.net/10803/670855.

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La inflamació és essencial en les respostes a les infeccions i danys perifèrics. Es poden obtenir beneficis de la inflamació si es controla durant un període de temps definit. La inflamació no regulada, sostinguda o excessiva és la causa principal de diferents neuropatologies. Al sistema nerviós central (SNC), la resposta neuroinflamatòria cerebral després d’una lesió cerebral traumàtica (TBI) s’ha caracteritzat en pacients i en diferents models animals experimentals com una de les principals causes de lesions secundàries que condueixen a la degeneració neuronal. La neuroinflamació es caracter

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Herber, Donna Lorraine. "Neuroinflammation in Alzheimer’s Disease: Characterization and Modification of the Response of Transgenic Mice to Intrahippocampal Lipopolysaccharide Administration." Scholar Commons, 2004. https://scholarcommons.usf.edu/etd/1076.

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Alzheimers disease (AD) is pathologically characterized by amyloid plaques, neurofibrillary tangles, inflammation, and neurodegeneration. According to the amyloid hypothesis of AD, the central mediating event of the disease is the deposition of amyloid. The inflammation hypothesis of AD states that it is the inflammatory response to plaques and tangles, rather than the actual lesions, which causes the disease. Studies described here combine the two approaches into a single model. Four studies are presented using a basic protocol of intrahippocampal lipopolysaccharide (LPS) injection to stimula

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Wang, Hui Hsin, and 王卉欣. "Reactive responses of astrocytes to pro-inflammatory mediators during neuroinflammation." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/52176794954952954694.

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博士<br>長庚大學<br>生物醫學研究所<br>98<br>Emerging evidence suggests that astrocytes undergo large morphologic and gene expression changes in response to central nervous system (CNS) injury. In the CNS pathology, uncontrolled metalloproteinase-9 (MMP-9) activity and nitric oxide (NO) production are implicated in the increase of blood–brain barrier (BBB) permeability, the entry of leukocytes into the CNS, and sustained inflammatory responses. After traumatic and ischemic brain insults, disruption of the BBB raises the possibility of exposing the CNS to oxidized low-density lipoprotein (oxLDL), a risk fact

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Ribeiro, Antónia Sofia Fortunato. "Exploring the expression of NLRP3 inflammasome in reactive astrocytes." Master's thesis, 2019. http://hdl.handle.net/10316/90067.

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Dissertação de Mestrado em Investigação Biomédica apresentada à Faculdade de Medicina<br>Neuroinflammation is an essential mechanism of innate immune defense in the CNS, but when unregulated it has been associated with the onset and progression of several pathologies, as neurodegenerative diseases. Astrocytes and microglia are the main immune effectors of the CNS and can become reactive when brain homeostasis is disrupted. In this way, these cells can contribute to the development of an inflammatory environment through the secretion of pro-inflammatory cytokines, like IL-1beta. Furthermore, as

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Wasserman, Jason. "Targeting Inflammation to Reduce Secondary Injury after Hemorrhagic Stroke." Thesis, 2008. http://hdl.handle.net/1807/11274.

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Intracerebral hemorrhage (ICH) is a devastating form of stroke that results from rupture of a blood vessel in the brain. Tissue inside the hematoma is irreversibly damaged soon after ICH onset and when this thesis research began, there was a dearth of information regarding pathological changes outside the hematoma. Inflammation is often proposed as a mechanism of injury, but very little information was available to show that inflammatory cells were in the right place at the right time to cause secondary brain injury. Using the collagenase-induced model of ICH, this work sought to better define

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Sequeira, Catarina Antunes. "Exploring A1 activation and miR-155 modulation in ALS spinal cord astrocytes." Master's thesis, 2018. http://hdl.handle.net/10362/52581.

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Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disorder, characterized by motor neurons (MN) loss in the brain and spinal cord (SC). Astrocyte reactivity and microglia activation account for neurodegeneration through the release of neurotoxins. Cytokines from activated microglia were shown to activate astrocytes and the inhibition of microglial microRNA(miRNA)-155 in ALS mice with G93A mutation in SOD1 gene (mSOD1) to recover their steady state phenotype and to attenuate disease progression. This thesis explored the reactive/inflammatory signature of ALS SC mSOD1 astrocytes, their

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Kalynovska, Nataliia. "Úloha angiotenzinových receptorů v modelu neuropatické bolesti." Master's thesis, 2012. http://www.nusl.cz/ntk/nusl-310569.

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Neuropathic pain is one of the most debilitating disorders. Currently available treatments for neuropathic pain are still unsatisfactory as they have only limited treatment effect and patients may suffer from unwanted side effects. Mechanism-based approaches to neuropathic pain treatment are considered to be more effective. Therefore multiple studies are dedicated to study the pathophysiological mechanisms of neuropathic pain. One of the possible underlying mechanism that causes neuropathic pain is neuroinflammation. Recent studies suggested that angiotensin II ( main effector molecule of the

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Ferreira, Sofia Gravanita. "Differences in AD astrocyte phenotypes and responses to microglial-derived cytokines." Master's thesis, 2018. http://hdl.handle.net/10362/52582.

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Dysregulated cross-talk between activated glia and neurons, mediated by exosomal trafficking, is a key mechanism in the spreading of neuroinflammation and in the exacerbation of the Alzheimer’s disease (AD) pathology. In AD patients, A1 reactive astrocytes are found in brain regions affected by neurodegeneration, and display a neurotoxic profile that is crucial for the disease progression. Despite its pivotal role in AD progression, the astroglial population remains strikingly under-investigated, mainly due to the lack of reliable experimental biological platforms to study glial cell function

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Chastre, Anne. "Le rôle de l’inflammation dans le développement des complications neurologiques associées à l’insuffisance hépatique aiguë chez la souris." Thèse, 2012. http://hdl.handle.net/1866/9886.

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L’insuffisance hépatique aiguë (IHA) se caractérise par la perte soudaine de la fonction hépatique résultant de la nécrose massive des hépatocytes en l’absence de pathologie hépatique préexistante. L’IHA s’accompagne de perturbations métaboliques et immunologiques qui peuvent entraîner l’apparition de complications périphériques et cérébrales telles qu’un syndrome de réponse inflammatoire systémique (SIRS), une encéphalopathie hépatique (EH), un œdème cérébral, une augmentation de la pression intracrânienne, et la mort par herniation du tronc cérébral. Les infections sont une complication fréq

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Neves, Sofia Pereira. "Studying the role of lipocalin-2 in the pathophysiology of multiple sclerosis: looking beyond the brain." Master's thesis, 2015. http://hdl.handle.net/1822/47233.

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Dissertação de mestrado em Ciências da Saúde<br>Multiple sclerosis (MS) is an immune-mediated demyelinating disease of the central nervous system (CNS), characterized by the presence of demyelination plaques, inflammation and gliosis that consequently lead to axonal damage. The sequence of events that leads to demyelination remains unclear and the pathophysiological mechanisms are diverse. Also, although this is a disease of the CNS, there is no doubt that, in terms of peripheral organs, the thymus, as the organ of T cell differentiation and maturation, plays an important role in the path

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(10725291), Priya Prakash. "Characterizing Microglial Response to Amyloid: From New Tools to New Molecules." Thesis, 2021.

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<p>Microglia are a population of specialized, tissue-resident immune cells that make up around 10% of total cells in our brain. They actively prune neuronal synapses, engulf cellular debris, and misfolded protein aggregates such as the Alzheimer’s Disease (AD)-associated amyloid-beta (Aβ) by the process of phagocytosis. During AD, microglia are unable to phagocytose Aβ, perhaps due to the several disease-associated changes affecting their normal function. Functional molecules such as lipids and metabolites also influence microglial behavior but have primarily remained uncharacterized to date.

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Shao-MingWang and 王紹銘. "Investigation of astrocytic CEBPD-mediated anti-apoptosis and reactive oxygen species formation in neuroinflammation." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/sqcgza.

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博士<br>國立成功大學<br>基礎醫學研究所<br>105<br>Neuroinflammation has been suggested to play a critical role in the pathogenesis of neurodegenerative disorders and central nervous system injury such as Alzheimer’s disease (AD) and spinal cord injury. Neuroinflammation can cause glia cell activation and produce inflammatory cytokines, especially astrocyte. Astrocytes are the principal cell type in the central nervous system (CNS) and are essential in normal brain tissue. They can secrete neurotrophic factors that support normal neuron function and survival. In contrast, astrocytes can be activated and cause

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Canedo, Teresa Correia Soares. "Unveiling the cellular and molecular players involved in methamphetamine - induced neuroinflammation: focus on astrocyte - microglial crosstalk." Doctoral thesis, 2022. https://hdl.handle.net/10216/139356.

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Clarkson, Melissa A. "Acute Astrogliosis and neurological deficits following repeated mild traumatic brain injury." Thesis, 2018. https://dspace.library.uvic.ca//handle/1828/10027.

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Mild traumatic brain injury (mTBI), often referred to as concussion, has become increasingly recognized as a serious health issue in the general population. The prevalence of mTBI in athletes, particularly repeated injuries in young athletes, is of great concern as injuries to the developing brain can have long-term detrimental effects. In this study we used a novel awake closed-head injury (ACHI) model in rodents to examine repeated mTBI (rmTBI), to determine if repeated injuries produced the neurological and molecular changes evident with human concussion. Animals were administered 4, 8, and

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Santos, Vanessa Filipa Coelho. "Effect of methylphenidate on blood-brain barrier function in health and attention deficit hyperactivity disorder." Doctoral thesis, 2018. http://hdl.handle.net/10316/79685.

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Tese de doutoramento do Programa Interuniversitário de Doutoramento em Envelhecimento e Doenças Crónicas, apresentada à Faculdade de Medicina da Universidade de Coimbra<br>Methylphenidate (MPH) is an amphetamine-like psychostimulant that has become the primary drug of choice for treating attention-deficit hyperactivity disorder (ADHD), a highly prevalent neuropsychiatric disorder with an onset in early childhood. ADHD includes behavioral and cognitive symptoms, such as inattention and/or impulsivity/hyperactivity. In more than 50% of children with ADHD, the symptoms persist into adolescence an

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LANA, DANIELE. "A study on cholinergic signal transduction pathways involved in short term and long term memory formation in the rat hippocampus. Molecular and cellular alterations underlying memory impairments in animal models of neurodegeneration." Doctoral thesis, 2014. http://hdl.handle.net/2158/850894.

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In this research project we studied signal transduction pathways triggered by cholinergic system and involved in short term and long term memory formation in the CA1 region of the rat hippocampus, focusing on mTOR pathway. We also evaluated memory impairments and molecular and cellular alterations of the neuron-astrocyte-microglia triad in the hippocampus, in three different animal models of neurodegeneration: normal brain aging, acute neuroinflammation induced by LPS infusion and chronic cerebral hypoperfusion induced by bilateral common carotid artery occlusion

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Leitão, Ricardo Alexandre Gomes. "Role of aquaporin-4 in methamphetamine-induced blood-brain barrier dysfunction and cerebral edema formation." Doctoral thesis, 2017. http://hdl.handle.net/10316/40920.

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Tese de doutoramento em Engenharia Biomédica, apresentada à Faculdade de Ciências e Tecnologia da Universidade de Coimbra<br>Methamphetamine (METH) is a powerful psychostimulant drug of abuse that has gained worldwide popularity, and its use originates severe health problems. Despite extensive characterization of METH-induced neurotoxicity over the last years, many questions remain unanswered. Several reports have demonstrated that oxidative stress, mitochondrial dysfunction, and neuroinflammation are some of the neurotoxic features of METH. More recently, it was shown that METH compromises th

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WIRTU, AMENU TOLERA. "OREXIN IN INFLAMMATION AND AGING-RELATED NEURODEGENERATIVE DISEASES." Doctoral thesis, 2015. http://hdl.handle.net/11562/915983.

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Questo progetto di dottorato deriva dall’ipotesi che i neuropeptidi rappresentati da orexina (OX)-A e-B (ipocretina-1 e – 2) e, in particolare, OX-A, costituiscano un bersaglio di segnali neuroinfiammatori, inclusa l’infiammazione di basso grado implicata nel processo cellulare e molecolare che sottende l’invecchiamento. Gli studi sperimentali che vengono qui presentati, eseguiti in topi adulti di divrese età inclusa l’età avanzata, sono stati mirati a testare la vulnerabilità dei neuroni orexinergici a uno stimolo infiammatorio esogeno rappresentato dalla somministrazione di lipopolisaccaride

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Meehan, Crystal Lea. "The role of early versus late gestational maternal immune activation in the aetiology of schizophrenia: establishing a rat model with a focus on cognitive symptomology and neuroinflammation." Thesis, 2018. http://hdl.handle.net/1959.13/1385728.

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Research Doctorate - Doctor of Philosophy (PhD)<br>Schizophrenia is a debilitating disorder of neurodevelopmental origins that likely stems from the cumulative action of a range of genetic and environmental factors. Epidemiological evidence has identified maternal infection during gestation as one significant environmental risk factor for the development of the disorder. Evidence from animal models has further validated the link between maternal immune activation (MIA) in the absence of an active infection and the later life development of schizophrenia-like pathology in the offspring. In part

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Cayrol, Romain. "Régulation moléculaire de la barrière hémo-encéphalique." Thèse, 2013. http://hdl.handle.net/1866/10359.

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La Sclérose en plaques (SEP) est une maladie auto-immune inflammatoire démyélinisante du système nerveux central (SNC), lors de laquelle des cellules inflammatoires du sang périphérique infiltrent le SNC pour y causer des dommages cellulaires. Dans ces réactions neuroinflammatoires, les cellules immunitaires traversent le système vasculaire du SNC, la barrière hémo-encéphalique (BHE), pour avoir accès au SNC et s’y accumuler. La BHE est donc la première entité que rencontrent les cellules inflammatoires du sang lors de leur migration au cerveau. Ceci lui confère un potentiel thérapeutique impo

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