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Relevant bibliographies by topics / Astrocyte neurodegeneration / Dissertations / Theses

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Dissertations / Theses on the topic 'Astrocyte neurodegeneration'

Author: Grafiati

Published: 2 June 2025

Last updated: 19 July 2025

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1

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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3

Efremova, Liudmila [Verfasser]. "Development of neuron-astrocyte co-culture system for mechanistic and pharmacological studies in neurodegeneration / Liudmila Efremova." Konstanz : Bibliothek der Universität Konstanz, 2015. http://d-nb.info/1081016922/34.

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4

Wang, Yongchao. "THE ROLE OF ENDOPLASMIC RETICULUM STRESS IN ETHANOL-INDUCED NEURODEGENERATION." UKnowledge, 2019. https://uknowledge.uky.edu/pharmacol_etds/33.

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Heavy ethanol use causes neurodegeneration manifested by neuronal loss and dysfunction. It is becoming imperative to delineate the underlying mechanism to promote the treatment of ethanol-induced neurodegeneration. Endoplasmic reticulum (ER) stress is a hallmark and an underlying mechanism of many neurodegenerative diseases. This study aims to investigate the role of ER stress in ethanol-induced neurodegeneration. In experimental design, adult mice were exposed to binge ethanol drinking by daily gavage for 1, 5, or 10 days and the response of ER stress was examined. We found the induction of E

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5

Di, Malta Chiara. "The analysis of a mouse model of Lysosomal Storage Disorder uncovers a role for astrocyte dysfunction in neurodegeneration." Thesis, Open University, 2012. http://oro.open.ac.uk/54503/.

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Astrocytes are the most abundant cellular population in the brain and their role in neurodegenerative processes is becoming increasingly appreciated. In my PhD project, I investigated the contribution of astrocytes to neurodegeneration in Multiple Sulfatase Deficiency (MS D), a severe Lysosomal Storage Disorder (LSD) caused by mutations in the Sulfatase Modifying Factor 1 (SUMF1) gene. Using Cre/Lox mouse models, I found that astrocyte-specific deletion of Sumf1 in vivo induced severe lysosomal storage and autophagy dysfunction with consequential cytoplasmic accumulation of toxic substrates. L

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6

CARUCCI, NICOLA MARIA. "Upon the way through which astrocytes sense and react to a reduction of extracellular Nerve Growth Factor level : NGF and Astrocytes in neurodegenerative disease models." Doctoral thesis, Scuola Normale Superiore, 2021. http://hdl.handle.net/11384/104404.

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7

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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8

Stone, Rebecca. "Glutathione release from astrocytes; characterization and implications for neurodegeneration." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395567.

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9

Maezawa, Izumi. "Glia-regulated, apolipoprotein E specific mechanisms of neuroprotection and neurodegeneration /." Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/6340.

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10

Jay, Taylor Reagan. "The TREM2 Receptor Directs Microglial Activity in Neurodegeneration and Neurodevelopment." Case Western Reserve University School of Graduate Studies / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=case1560181547156823.

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11

Avola, Rosanna. "Dynamic expression of aquaporins in physiological and pathophysiological in vitro models." Doctoral thesis, Università di Catania, 2017. http://hdl.handle.net/10761/3620.

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Water is the main component of biological fluids and a prerequisite of all organisms living. In 1987, Agre isolated a new integral membrane protein acting as a channel that mediates the water flux and uncharged solutes across biological membranes. This protein was called aquaporin1 and ever since its discovery, more than 300 homologues have been identified in animal, bacteria and plant. In human have been discovered 13 aquaporins (AQPs) isoform (AQP0-AQP12) widely distributed in various epithelia and endothelia where are important actors of fluid homeostasis in secretory and absorptive process

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12

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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13

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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14

Engler, Henry. "PET and the Multitracer Concept: An Approach to Neuroimaging Pathology." Doctoral thesis, Uppsala University, Department of Medical Sciences, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8687.

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<p>Patients suffering from different forms of neurodegenerative diseases, such as: Creutzfeldt Jacob Disease (CJD), Alzheimer disease (AD), mild cognitive impairment (MCI), frontotemporal dementia and Parkinson’s disease (PD) were examined with Positron Emission Tomography (PET) and the combination of different radiotracers: <sup>15</sup>O-water, N-[<sup>11</sup>C-methyl]-L-deuterodeprenyl (DED), [<sup>18</sup>F] 2-fluorodeoxyglucose: (FDG), N-methyl-[<sup>11</sup>C]2-(4-methylaminophenyl)-6-hydroxybenzothiazole (PIB) and L-[<sup>11</sup>C]-3,4-dihydroxiphenyl-alanine (DOPA). The radiotracers

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15

Guillemaud, Océane. "Hétérogénéité de la réactivité astrocytaire dans la maladie d'Alzheimer." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL003.

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Les astrocytes sont essentiels au fonctionnement du cerveau. Dans les maladies neurodégénératives comme la maladie d’Alzheimer (MA), les astrocytes deviennent réactifs. Le rôle des astrocytes réactifs (AR) dans la MA reste débattu.Nous avons utilisé une approche virale permettant de moduler sélectivement les AR, in vivo, par ciblage de la voie JAK2-STAT3 dans deux modèles murins de la MA. Nous observons que l’inhibition des AR améliore la pathologie amyloïde et l’apprentissage spatial chez les souris APP/PS1dE9 (Ceyzériat et al., 2018). Dans les souris 3xTg-AD, la modulation des AR améliore la

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16

Fernández, Carasa Irene. "Investigating the role of mitochondrial dysfunction in the pathogenesis of Parkinsons´s disease using patient-specific derived astrocytes." Doctoral thesis, Universitat de Barcelona, 2021. http://hdl.handle.net/10803/673716.

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Parkinson’s disease (PD) is an incurable, chronically progressive disorder of old age leading to premature invalidity and death. Clinically, PD is characterized by classical motor syndrome linked to a progressive loss of dopamine-containing neurons (DAn) in the substantia nigra pars compacta, and disabling non-motor symptoms related to extranigral lesions. The identification of several genes associated to familiar PD have brought considerable insight into underlying pathogenic mechanisms. However, the unknown etiology of the sporadic forms (90% of patients) and the emerging view that non-neur

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17

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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18

Vidović, Natascha [Verfasser], and Richard [Akademischer Betreuer] Dodel. "Investigating the role of glial cells in neurodegenerative disorders by depleting astrocytes and oligodendrocytes in a model of amyloid-beta induced cytotoxicity in organotypic hippocampal slice cultures / Natascha Vidovic ; Betreuer: Richard Dodel." Marburg : Philipps-Universität Marburg, 2021. http://d-nb.info/1235139328/34.

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19

Curry, Nathan. "Development and application of correlative STED and AFM to investigate neuronal cells." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/274579.

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Over the past three decades in cellular neuroscience there has been a shift towards the view of the 'tripartite synapse', where, astrocytes -- as well as the pre-synapse and post-synapse -- are involved in synaptic signalling. The migration of astrocytes to form branched networks in the brain is, therefore, of great interest in understanding brain development and neuronal function. Migration is a complex interplay between cytoskeletal reorganisation and cell mechanical stiffness. In order to improve understanding of this process, correlative measurements of cytoskeletal organisation and mechan

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20

Tan, Vanessa. "Identification of biomarkers for MND, and understanding the potential role of the cyanotoxin BMAA in neurodegeneration Involvement of Quinolinic Acid in the Neuropathogenesis of amyotrophic lateral sclerosis Detection of the Cyanotoxins L-BMAA Uptake and Accumulation in Primary Neurons and Astrocytes." Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS590.

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La Sclérose Latérale Amyotrophique (SLA) est une maladie neurodégénérative dévastatrice dont les causes sont inconnues et pour laquelle il n’existe aucun traitement ni marqueur spécifique. Dans ce contexte, nous avons étudié le rôle de la voie métabolique des kynurénines impliquée dans la production de métabolites neuroactifs qui peuvent être immunomodulateurs, neuroprotecteurs ou à l’inverse neurotoxiques. Dans une étude longitudinale du sérum de 66 patients atteints de SLA, nous avons évalué le profil de 10 métabolites de la voie des kynurénines par chromatographie HPLC et spectrographie GC/

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21

Sirisi, Dolcet Sònia. "Bases moleculars de la Leucoeocefalopatia Megalencefàllca amb Quists subcorlicals. Utilització de models animals i cel·lulars." Doctoral thesis, Universitat de Barcelona, 2014. http://hdl.handle.net/10803/284761.

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La Leucoencefalopatia Megalencefàlica amb quists subcorticals, també anomenada MLC, és un tipus rar de leucodistròfia vacuolitzant. Actualment encara es desconeix el mecanisme fisiopatològic de la malaltia, i per tant ni hi ha cap tractament possible per als pacients. S’han descrit dos gens implicats en la malaltia MLC. El primer gen descobert s’anomena MLC1 i codifica per una proteïna de membrana que porta el mateix nom. El segon gen s’anomena GLIALCAM i codifica per una proteïna transmembrana de tipus I que també porta el mateix nom. S’ha decrit que la proteïna GlialCAM actua com a subunit

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22

Arnedo, Llena Tanit. "Paper del canal de clorur CIC-2 en les patologies de la mielina." Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/310220.

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La Leucoencefalopatia Megalencefàlica amb Quists subcorticals (MLC) és un tipus rar de leucodistròfia vacuolitzant de progressió lenta, que presenta com a principals característiques clíniques macrocefàlia acusada durant els primers anys de vida, deteriorament de les funcions motores, epilèpsia i retard mental de grau mig. Actualment encara es desconeix el mecanisme fisiopatològic de la malaltia, i per tant ni hi ha cap tractament possible per als pacients. S’han descrit dos gens implicats en la malaltia MLC. El primer gen descobert s’anomena MLC1 i codifica per una proteïna de membrana que po

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23

Norante, Rosa Pia. "Studying alterations of Ca2+ homeostasis in in vitro cell models of Amyotrophic Lateral Sclerosis." Doctoral thesis, Università degli studi di Padova, 2017. http://hdl.handle.net/11577/3425364.

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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the selective death of motor neurons (MNs). The mechanism of MN demise, however, is poorly understood, and no effective treatment is yet available. In most cases ALS occurs sporadically, but 10% of cases show a familial history and about 20% of these familial ALS (fALS) are caused by a mutation in the superoxide dismutase 1 (SOD1) gene. In particular, expression of the fALS-related SOD1(G93A) mutant in transgenic (Tg) mice closely resembles human disease. Recent research has found that mutant SOD1 (mSOD1)

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24

Ugbode, Christopher I., I. Smith, B. J. Whalley, W. D. Hirst, and Marcus Rattray. "SHH signalling mediates astrocyte crosstalk with neurons to confer neuroprotection." 2017. http://hdl.handle.net/10454/12042.

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Yes<br>Sonic Hedgehog (SHH) is a glycoprotein associated with development that is also expressed in the adult CNS and released after brain injury. Since the SHH receptors PTCH1 (patched homolog-1) and SMO (Smoothened) are highly expressed on astrocytes, we hypothesised that SHH regulates astrocyte function. Primary mouse cortical astrocytes derived from embryonic (E15) Swiss mouse cortices, were treated with two chemically distinct agonists of the SHH pathway, which caused astrocytes to elongate and proliferate. These changes are accompanied by decreases in the major astrocyte glutamate transp

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25

Spilsbury, A., D. Vauzour, J. P. E. Spencer та Marcus Rattray. "Regulation of NF-κB activity in astrocytes: effects of flavonoids at dietary-relevant concentrations". 2012. http://hdl.handle.net/10454/7804.

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-<br>Neuroinflammation plays an important role in the progression of neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease. Sustained activation of nuclear transcription factor κB (NF-κB) is thought to play an important role in the pathogenesis of neurodegenerative disorders. Flavonoids have been shown to possess antioxidant and anti-inflammatory properties and we investigated whether flavonoids, at submicromolar concentrations relevant to their bioavailability from the diet, were able to modulate NF-κB signalling in astrocytes. Using luciferase reporter assays, we fo

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26

Ribeiro, Mariana Messias de Jesus Rufino. "Astrocyte-specific Transcriptomic Response to PGC-1a Isoforms." Master's thesis, 2018. http://hdl.handle.net/10451/40028.

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Tese de mestrado, Ciências Biofarmacêuticas, Universidade de Lisboa, Faculdade de Farmácia, 2018<br>Peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α) transcriptional coactivators are key regulators of energy metabolism-related genes and are expressed in energy-demanding tissues. There are several PGC-1α variants that exert differential and specific biological functions. In the brain, PGC-1α1 has been implicated in reactive oxygen species detoxification but our understanding of the role of the other isoforms is far from complete. Previous results have shown that PGC-1α is

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27

Ugolini, Filippo, Maria Grazia Giovannini, and Lana Daniele. "A study on different patterns of alteration of the neuron-glia interplay in experimental models of neurodegeneration." Doctoral thesis, 2020. http://hdl.handle.net/2158/1214966.

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28

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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29

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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30

Steele, Megan. "Effect of proinflammatory activation on the neurosupportive functions of astrocytes." Thesis, 2011. http://handle.uws.edu.au:8081/1959.7/506974.

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A complex relationship exists between astrocytes and neurons involving astrocytic uptake of glucose and glutathione (GSH) precursors (cysteine, glycine and glutamate) and the release of lactate and GSH, which are taken up by neurons, either directly or after extracellular degradation. This metabolic exchange between astrocytes and neurons is vital to normal neuronal functions including GSH-dependent cellular antioxidant defence. It is therefore hypothesised that a breakdown in astroglial-neuronal interaction, due to chronically activated astrocytes altering their metabolic phenotype, might lea

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Peake, Kyle. "Cholesterol metabolism in the Niemann-Pick Type C brain." Phd thesis, 2011. http://hdl.handle.net/10048/1696.

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Niemann-Pick Type C (NPC) disease is an autosomal recessive disorder that results in accumulation of unesterified cholesterol in late endosomes/lysosomes (LE/Ls), leading to progressive neurodegeneration and premature death. Microglia are resident immune cells of the central nervous system, which upon activation can secrete potentially neurotoxic molecules such as tumor necrosis factor-alpha (TNFα). Inappropriate activation of microglia has been implicated in NPC disease. Primary microglia cultures from the cerebral cortex of Npc1-/- mice have an altered cholesterol distribution characteristi

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32

Kaiser, Melanie. "Differentielle Expression und Funktion eines glialen Kaliumkanals (K_ir4.1, KCNJ10) im Rückenmark und Bedeutung in einem neurodegenerativen Krankheitsmodell." Doctoral thesis, 2008. http://hdl.handle.net/11858/00-1735-0000-0006-ACFA-4.

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Innerhalb des letzten Jahrzehnts wurde immer deutlicher, dass einwärts-gleichrichtende Kaliumkanäle (Kir) neben ihrer klassischen Rolle im Aufbau und der Konstanthaltung des Ruhemembranpotentials weitere zellspezifische Aufgaben erfüllen.In der vorliegenden Arbeit konnte mittels transgener Maustechnologie gezeigt werden, dass Kir4.1 früh postnatal zunächst Zellkörper-assoziiert auf Oligodendrozyten in der weißen Substanz des Rückenmarks exprimiert wird. Im weiteren Verlauf der Entwicklung

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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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