Dissertations / Theses on the topic 'Neuroprotective proteins'
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Wagstaff, Marcus James Dermot. "The neuroprotective effect of the heat shock proteins." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267150.
Full textAron, Badin Romina. "Neuroprotective effects of heat shock proteins in experimental ischaemia : an MRI study." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1444501/.
Full textAvery, Michelle A. "Axon Death Prevented: Wlds and Other Neuroprotective Molecules: A Dissertation." eScholarship@UMMS, 2010. https://escholarship.umassmed.edu/gsbs_diss/520.
Full textBoulos, Sherif. "Identification and characterisation of potential neuroprotective proteins induced by erythropoietin (EPO) preconditioning of cortical neuronal cultures." University of Western Australia. School of Biomedical and Chemical Sciences, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0128.
Full textLee, Christopher James. "Neuroprotective effects of overexpression of the inhibitor of apoptosis proteins in the quinolinic acid model of excitotoxic injury." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0020/MQ48164.pdf.
Full textAboonq, Moutasem Salih. "Activity dependent neuroprotective protein (ADNP) expression and functions." Thesis, University of Liverpool, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.540017.
Full textLin, Tse-Shen. "Prion protein topologies and the effect on its neuroprotective function." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=18773.
Full textLa forme normale du prion (PrP) est exprimée de façon omniprésente mais elle est particulièrement abondante dans le cerveau. Cependant, la fonction physiologique principale du PrP reste indéfinie. Récemment, il a été démontré que PrP empêche la mort cellulaire causée par Bax (Bcl-2-associated protein X) en inhibant le changement de conformation initial de Bax, à partir duquel le Bax cytosolique est converti en protéine pro-apoptotique (Roucou et al., 2005). Afin de mieux déterminer la forme et la localisation sous-cellulaire de PrP ayant une fonction anti-Bax, nous avons co-exprimé divers mutants de PrP du hamster syrien (SHaPrP), lesquels favorisent des topologies et des localisations sous-cellulaires spécifiques de PrP, avec la construction pro-apoptotique Bax marquée à son bout N-terminal par la protéine fluorescente verte (EGFP-Bax), et ce, dans la lignée cellulaire MCF-7 et dans les neurones humaines primaires. Les mutants PrP qui favorisent les formes transmembranaire de PrP perdent leur fonction anti-Bax, tandis que ceux qui produisent exclusivement du PrP sécrété ou cytosolique (CyPrP) retiennent une protection comparable à celle du PrP sauvage retrouvée dans les deux types de cellules. De plus, la co-expression de CyPrP avec ces mutants récupère la fonction anti-Bax. L'ajout du PrP extracellulaire ne soutient que de façon minimale la fonction anti-Bax. Par conséquent, ces résultats indiquent que le CyPrP est la forme prédominante de PrP possédant une fonction anti-Bax. Nous avons exclut précédemment la nécessité de présence de d'autres membres de la famille Bcl-2 dans la fonction anti-Bax. Ici, nous n'avons pas pu co-immunoprécipiter PrP et Bax, ce qui indique que la fonction anti-Bax du PrP ne peut être pas attribuée à une interaction directe entre PrP et Bax, dans le cytosol. Nous concluons donc que PrP exercerait son effet sur Bax via un interagisseur cytosolique.
Johnson, Erik Andrew. "Survivin expression after traumatic brain injury potential roles in neuroprotection /." [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0008337.
Full textTypescript. Title from title page of source document. Document formatted into pages; contains 87 pages. Includes Vita. Includes bibliographical references.
Gustafsson, Helena. "Uncoupling Proteins : Regulation by IGF-1 and Neuroprotection during Hyperglycemia in Vitro." Doctoral thesis, Stockholm : Institutionen för neurokemi och neurotoxikologi, Univ, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-121.
Full textSakthivelu, Vignesh. "Functional characterization of Shadoo, a PrP-like protein with neuroprotective activity." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-144326.
Full textGains, Malcolm J. "The in vivo neuroprotective role of the normal cellular prion protein /." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103158.
Full textThe first paradigm involved an external insult (ethanol injection) to 7 day old mice, which induces massive Bax-mediated neuronal death. We then quantified the number of active caspase 3 positive cells, as a downstream marker of Bax activation, induced in mice on various genetic backgrounds, PrP overexpressors (PrpOexp), PrP wild-type (PrP+/+ ) and PrP knockout (PrP0/0). We also examined Bax activation by immunoprecipitation of subcellular fractions, as well as total Bax activation and cytochrome c release directly in ex-vivo mouse brains. In addition, we examined the insertion of active Bax into the mitochondrial membrane, also using subcellular fractionation.
The second paradigm involves an internal insult (physiological Bax-mediated neuronal death during embryonic development). This insult results in massive Bax-mediated cell death in embryonic mice that do not express the natural antagonist of Bax i.e. BClxL. We have therefore created 3 lines of transgenic mice expressing Syrian Hamster PrP (SHaPrP) under the control of the Bclx promoter, to cross with Bclx+/- mice to see if the SHaPrP can assume the role of Bclx in Bclx knockout mice and rescue the neuronal cell death.
In the first paradigm, greater numbers of neurons undergoing apoptosis following ethanol insult were seen in PrP0/0 than in PrP +/+ mice, although the differences were not statistically significant. The ex-vivo examination of mouse brains did not provide definitive results.
In the second paradigm, 3 lines of transgenic mice have been created and are in various stages of breeding to obtain the required genotypes to test our hypothesis. The level of expression of SHaPrP in these mice is below the level of detection via western blot or immunoprecipitation.
The trend shown in our results suggests that in vivo, PrPC may provide some protection for neurons from Bax-mediated cell death as a result of an external insult. Research is ongoing to see if PrPC can protect neurons in vivo against developmental Bax-mediated cell death. The work presented here highlights the variability and technical difficulty inherent with in vivo studies, particularly when the available knowledge of the biochemical pathways involved is incomplete.
Piorkowska-Stanco, Katarzyna. "DJ-1 as a neuroprotective protein in models of Parkinson's disease /." [S.l.] : [s.n.], 2007. http://library.epfl.ch/theses/?nr=3926.
Full textGennet, Nicole. "Activity dependent neuroprotective protein : initial characterisation of its role in physiology." Thesis, University of Liverpool, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.423968.
Full textYang, Guang. "Palmitoyl-proteins : regulators of neuronal functions and potential targets for neuroprotection." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/38155.
Full textRahim, Titissa. "Investigating the regulation of ARNT2, a neuroprotective protein, in models of multiple sclerosis." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/58253.
Full textMedicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
Davis, Stephanie. "Leukemia Inhibitory Factor as a Neuroprotective Agent against Focal Cerebral Ischemia." Scholar Commons, 2016. http://scholarcommons.usf.edu/etd/6218.
Full textMaezawa, 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.
Full textBenn, Susanna Clare. "Neuroprotection by heat shock protein 27 in sensory and motor neurons." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271424.
Full textKelly, Stephen. "Neuroprotection and functional alterations in mice over-expressing heat shock protein 70i." Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327580.
Full textAli, Yousuf O. "The Mechanism of Neuroprotection Mediated By Nicotinamide Mononucleotide Adenylyl Transferase (NMNAT)." Scholarly Repository, 2011. http://scholarlyrepository.miami.edu/oa_dissertations/633.
Full textLee, Bo Young. "Signaling events in activity dependent neuroprotection, neurodegeneration, and synaptic plasticity." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1180458484.
Full textHo, Wing-Lok Philip. "The role of neuronal mitochondrial uncoupling proteins in MPP+ -Induced toxicity : a potential for neuroprotection in Parkinsonism." Click to view the E-thesis via HKUTO, 2004. http://sunzi.lib.hku.hk/hkuto/record/B31498966.
Full textHo, Wing-Lok Philip, and 何永樂. "The role of neuronal mitochondrial uncoupling proteins in MPP+ -Induced toxicity: a potential for neuroprotection in Parkinsonism." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B31498966.
Full textSakthivelu, Vignesh [Verfasser], and Jörg [Akademischer Betreuer] Tatzelt. "Functional characterization of Shadoo, a PrP-like protein with neuroprotective activity / Vignesh Sakthivelu. Betreuer: Jörg Tatzelt." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2012. http://d-nb.info/1023661055/34.
Full textLorente, Picon Marina. "Neuroprotective effect of stomatin-like protein 2 overexpression in A53T-a-synuclein parkinson disease mice model." Master's thesis, Université Laval, 2020. http://hdl.handle.net/20.500.11794/66338.
Full textYau, Suk-yu. "Neuroprotective effects of physical exercise on stressed brain : its relationship to hippocampal neurogenesis and dendritic remodeling /." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B4322376X.
Full textCampelo, Marcio Wilker Soares. "Preconditioning with nitrosyl ruthenium promotes neuroprotection involving protein kinase in rat brain in vivo." Universidade Federal do CearÃ, 2015. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=16083.
Full textBackground and purpose - The NO donors can decrease neuronal injury during cerebral ischemia and reperfusion (I/R) by increasing the blood flow to the brain. The objective of this study is to study whether a new nitrosyl ruthenium complex makes some effect during I/R and if involves protein kinases. Methods - Used 180 male rats, Wistar rats, with an average weight of 290.27 g, distributed 6 groups: Sham 1h, saline + ischemia/reperfusion 1h, Ru-bpy ischemia/reperfusion 1h, Sham 24h, saline + ischemia/reperfusion 24h, Ru-bpy ischemia/reperfusion 24h. Used global cerebral ischemia model incomplete, with occlusion of bilateral common carotid artery and administration of SF or Rut-bpy in their respective groups by intraperitoneal way. At the end of the experiment, the animals were decapitated and the brain removed to be evaluated to the area of injury by histology with H&E, immunohistochemistry, quantification of brain swelling, nitrite, immunoassay for kinases. During the experiment (phase of ischemia and first hour of reperfusion) PAM of animals was monitored. Results: Decreased number of neurons reds and edema in brain tissue in animals preconditioned with nitrosyl ruthenium. PAM variation was lower in animals treated with Ru-bpy the end of ischemia and early reperfusion. Inhibition of NF-kB. Activates the kinase protein Akt, Erk 1/2, p70S6 and CREB, with inhibition of JNK protein.Conclusion: The Rut-bpy has protective effect during neuronal event of I/R supported by 24h and keeping PAM more stable during the beginning of reperfusion. Involving the protein kinase.
IntroduÃÃo e objetivo: Doadores de NO (Ãxido nÃtrico) podem diminuir a lesÃo neuronal durante a isquemia/reperfusÃo (I/R) cerebral experimental por aumento do fluxo sanguÃneo cerebral. O objetivo deste estudo foi avaliar se um novo doador de NO complexo nitrosil rutÃnio (Ru-bpy) apresenta algum efeito durante I/R e se envolve proteÃnas quinases. MÃtodo: Foram utilizados 180 ratos machos, da linhagem Wistar, com peso mÃdio de 290.27 g, distribuÃdos 6 grupos: Sham 1h, soluÃÃo salina + isquemia/reperfusÃo 1h, Ru-bpy + isquemia/reperfusÃo 1h, Sham 24h, soluÃÃo salina + isquemia/reperfusÃo 24h, Ru-bpy + isquemia/reperfusÃo 24h. Utilizado o modelo de isquemia cerebral global incompleta, com oclusÃo da artÃria carÃtida comum bilateral e administraÃÃo do SF ou Rut-bpy em seus respectivos grupos via intraperitoneal 30 minutos antes do inicio do pinÃamento das carÃtidas comuns. ApÃs 30 minutos de isquemia. No final do experimento os animais foram decapitados e o cÃrebro retirado para ser avaliado à Ãrea de lesÃo por histologia com H&E, imunohistoquÃmica, quantificaÃÃo de edema cerebral, nitrito, imunoensaio para quinases. Durante o experimento (fase de isquemia e primeira hora de reperfusÃo) a pressÃo artÃrial mÃdia (PAM) dos animais foi monitorizada. Resultados: DiminuiÃÃo do nÃmero de neurÃnios eosinofÃlicos e do edema no tecido cerebral nos animais prÃ-condicionados com nitrosil rutÃnio. A variaÃÃo da PAM foi menor nos animais tratados com Ru-bpy ao final da isquemia e inÃcio da reperfusÃo. InibiÃÃo do NF-kB. AtivaÃÃo das proteÃnas quinase AKT, P70S6, ERK 1/2 e CREB, com inibiÃÃo da proteÃna JNK. ConclusÃo: O Rut-bpy tem efeito protetor neuronal durante evento de I/R sustentado por 24h mantendo a PAM mais estÃvel durante o inÃcio da reperfusÃo. Envolvendo a via das proteÃnas quinases.
Yau, Suk-yu, and 邱淑瑜. "Neuroprotective effects of physical exercise on stressed brain : its relationship to hippocampal neurogenesis and dendritic remodeling." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hdl.handle.net/10722/210329.
Full textKundu, Arpita [Verfasser], Donat [Gutachter] Kögel, and Jochen [Gutachter] Klein. "The role of the amyloid precursor protein (APP) in protein homeostasis and neuroprotection / Arpita Kundu ; Gutachter: Donat Kögel, Jochen Klein." Frankfurt am Main : Universitätsbibliothek Johann Christian Senckenberg, 2017. http://d-nb.info/114052576X/34.
Full textDescamps, Elodie Vamecq Joseph. "La protéine disulfide isomérase et l'ischémie cérébrale une voie de neuroprotection ? /." [S.l.] : [s.n.], 2009. http://tel.archives-ouvertes.fr/tel-00399737/fr.
Full textDavis, Laurie Michelle Helene. "THE UNDERLYING MECHANISM(S) OF FASTING INDUCED NEUROPROTECTION AFTER MODERATE TRAUMATIC BRAIN INJURY." UKnowledge, 2008. http://uknowledge.uky.edu/gradschool_diss/673.
Full textWelin, Dag. "Neuroprotection and axonal regeneration after peripheral nerve injury." Doctoral thesis, Umeå : Umeå university, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-32819.
Full textSousa, Rafael Augusto Teixeira de. "Fisiopatologia do Transtorno de Humor Bipolar e efeito do tratamento com lítio: enfoque em neuroproteção e função mitocondrial." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5142/tde-05052014-142705/.
Full textBackground: Several evidences point to a role for mitochondrial dysfunction in Bipolar Disorder (BD), but few is known about it on short-term BD. In mitochondria the electron transport chain (ETC) acts jointly with citric acid cycle to produce energy, but it is not clear if they are altered in BD. Mitochondrial DNA (mtDNA) encodes several ETC proteins and is associated with oxidative stress, but it was never evaluated in BD in vivo. Oxidative stress is associated with BD and with mitochondrial dysfunction, but few is known about the activities of antioxidant enzymes in short-term BD. Nitric oxide (NO) is a molecule with neuromodulatory effects, but with an unclear role in BD. Lithium is a gold-standard treatment for BD, which has shown neuroprotective effects. However, few is known about lithium effect on ETC, citric acid cycle, mtDNA content, and NO regulation in humans. Also, lithium\'s antioxidant role in BD is unclear. Methods: Patients with BD depression (n=31) unmedicated in majority (84%) received lithium treatment for 6 weeks. Before and after treatment, in leukocytes the activities of ETC complex I-IV, citrate synthase, succinate dehydrogenase, and malate dehydrogenase, and mtDNA content were evaluated; in plasma, NO levels, thiobarbituric acid reactive substances (TBARS), the activities of catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD), and SOD/CAT ratio were evaluated. Bipolar depression patients were compared with 28 healthy controls. Results: When compared with controls, BD patients showed an increase in GPx (p < 0.001) and CAT (p=0.005) and a decrease in SOD/CAT (p=0.001), but showed no difference for other biomarkers. Patients with BD I showed a decrease in citrate synthase (p=0.02) and a slight decrease in mtDNA content (p=0.05) when compared to BD II; mtDNA content was slightly decreased in BD I compared to controls (p=0.05). From baseline to endpoint, there was an increase in ETC complex I activity (p=0.02), a decrease in TBARS (p=0.02) and SOD (p=0.03) and an increase in NO (p=0.02), without change in other parameters. After treatment, TBARS was decreased in responders compared to non-responders (p=0.02) and decreased in BD II compared to BD I (p=0.04). Discussion: In short-term BD few alterations were observed on biomarkers. The findings suggest increase on CAT and GPX in short-term bipolar depression and mitochondrial content decrease in BD I when compared to BD II, which deserve other studies for confirmation. The results reinforce a lithium\'s neuroprotective role and suggest that lithium increases ETC complex I activity and NO levels in bipolar depression. Moreover, lithium reinforced its role as antioxidant and as a modulator of antioxidant enzymes in BD
Choi, Christopher J. "Interaction of prion protein with divalent metals possible role in neuroprotection and neurodegeneration in prion disease model /." [Ames, Iowa : Iowa State University], 2007.
Find full textLai, Sau-wan. "Investigating beta-amyloid peptide neurotoxicity from neuronal apoptosis to endoplasmic reticulum collapse translational research back to basic science research /." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B41633702.
Full textDescamps, Elodie. "La protéine disulfide isomérase et l'ischémie cérébrale : une voie de neuroprotection ?" Phd thesis, Lille 2, 2009. http://www.theses.fr/2009LIL2S009.
Full textGupte, Raeesa Prashant. "Phosphoregulation of somatodendritic voltage-gated potassium channels by pituitary adenylate cyclase-activating polypeptide." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/5766.
Full textHata, Masayuki. "KUS121, a VCP modulator, attenuates ischemic retinal cell death via suppressing endoplasmic reticulum stress." Kyoto University, 2018. http://hdl.handle.net/2433/232075.
Full textMontecinos, Carla. "AMPA receptor stabilization mediated by non-canonical Wnt signaling protects against Aβ42 oligomers synaptotoxicity." Thesis, Bordeaux, 2018. http://www.theses.fr/2018BORD0268.
Full textAMPARs (AMPARs) are responsible for most fast excitatory synaptic transmission in the central nervous system, including hippocampal neurons studied here. AMPARs are highly dynamic in the plasma membrane. Within dendritic spines, they move by membrane trafficking between intracellular compartments and the plasma membrane. Once at the surface, they move through lateral brownian diffusion and can reversibly anchor to postsynaptic density proteins or return to endocytic compartments. Aβ oligomers increase endocytosis of AMPARs, diminish dendritic spine density and cause overall failures in excitatory transmission. These effects, among others, are englobed in the term “Aβ oligomers synaptotoxicity” and are a main focus on the study of Alzheimers disease ethiology. On the contrary, Wnt5a - an endogenous Wnt ligand known to activate the non-canonical pathway in hippocampal neurons - generates an increase in excitatory currents and in clusters of PSD95 and protects neurons against Aβ oligomers synaptotoxicity. Given the fact that Wnt5a seems to counteract the distresses caused by Aβ oligomers, we proceeded to study the mechanism through which Wnt5a protects from Aβ oligomers synaptotoxicity. This led us to evaluate the effect of Wnt5a on one of the important factors in glutamatergic transmission, i.e. AMPAR receptor dynamics. By using super-resolution microscopy in live and fixed hippocampal neurons, we found that Wnt5a modulates the dynamic and localization of AMPARs. Specifically, Wnt5a stabilizes AMPARs in synaptic and extrasynaptic sites. This correlates with an increase in co-localization and interaction between GluA2 and PSD95. These effects are exerted only by non-canonical activation of Wnt signaling, through Wnt5a ligand and not by the canonical effects of Wnt7a. Interestingly, pre-incubation of Wnt5a prevents toxicity of Aβ oligomers and maintains basal AMPARs dynamics. Our data suggest that Wnt5a prevents Aβ oligomers effects by promoting their stabilization in synaptic sites
Los receptores AMPA (AMPARs) son los principales responsables de la respuesta excitatoria rápida en el sistema nervioso central, incluyendo neuronas hipocampales, estudiadas en esta tesis. A diferencia de otros receptores glutamatérgicos, los AMPARs son altamente dinámicos. Dentro de las espinas dendríticas, se pueden mover hacia y desde compartimentos endocíticos y hacia la membrana plasmática. Una vez en la superficie, a través de difusión lateral, se pueden anclar a proteínas de la densidad postsináptica o regresar a compartimentos endocíticos. Por otro lado, los oligómeros Aβ (oAβ) aumentan la endocitosis de AMPARs, disminuyen la densidad de espinas dendríticas y causan una falla generalizada de la transmisión sináptica excitatoria. Estos efectos, entre otros, se engloban en el término “sinaptotoxicidad por oAβ” y es uno de los principales puntos de estudio en la etiología de la enfermedad de Alzheimer. Al contrario, Wnt5a un ligando endógeno conocido por activar la vía no canónica en neuronas hipocampales, genera un aumento en corrientes excitatorias y en los clusters de PSD95 y protege a las neuronas contra la sinaptotoxicidad causada por oAβ. Debido a esto, procedimos a estudiar el mecanismo por el cual Wnt5a protege de la sinaptotoxicidad causada por Aβ. Esto nos llevó a evaluar los efectos de Wnt5a en uno de los principales factores en la transmisión glutamatérgica, la dinámica de los AMPARs. Con el uso de microscopía de super-resolución en neuronas hipocampales vivas, encontramos que Wnt5a modula la dinámica y localización de los AMPARs. Específicamente, Wnt5a estabiliza los AMPARs en espinas y dendritas. Lo cual se correlaciona con un aumento en la co-localización e interacción entre GluA2 y PSD95. Estos efectos son causados únicamente por la activación no-canónica de la vía Wnt, a través del ligando Wnt5a y no por los efectos canónicos de Wnt7a. De manera interesante, la pre-incubación de Wnt5a previene la toxicicidad de los oligómeros Aβ y mantiene la dinámica basal de los AMPARs. Esta data sugiere que Wnt5a promueve la estabilización de AMPARs, previniendo los efectos synaptotóxicos de los oAβ
Bertling, Frederik [Verfasser], and Ursula [Akademischer Betreuer] Felderhoff-Müser. "Tumor necrosis factor-inducible gene 6 protein : A novel neuroprotective factor against inflammation-induced developmental brain injury / Frederik Bertling ; Betreuer: Ursula Felderhoff-Müser." Duisburg, 2017. http://d-nb.info/1143518705/34.
Full textJiang, Lixian. "Interactions of Neurons, Astrocytes and Microglia with HUCB Cell Populations in Stroke Models: Migration, Neuroprotection and Inflammation." [Tampa, Fla] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002552.
Full textSuttkus, Anne, S. Rohn, Solveig Weigel, P. Glöckner, Thomas Arendt, and Markus Morawski. "Aggrecan, link protein and tenascin-R are essential components of the perineuronal net to protect neurons against iron-induced oxidative stress." Universitätsbibliothek Leipzig, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-148326.
Full textLeva, Géraldine. "Neuroprotection dans des modèles animaux de la sclérose en plaques : évaluation pluridisciplinaire de la capacité du XBD173, un ligand du translocator protein, à améliorer les symptômes cliniques et les marqueurs neuropathologiques." Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ076/document.
Full textMultiple sclerosis (MS) is a chronic inflammatory autoimmune disease affecting the central myelin. Progress has been made for MS treatment, but effective neuroprotective drugs against MS-evoked axonal damages and severe disability are still missing. This thesis assessed the potential of XBD173, a ligand of the translocator protein controlling neurosteroidogenesis and neuroinflammation, to improve symptoms in the proteolipid protein-induced MS model (EAE-PLP mice) that mimics the relapsing-remitting form affecting 85% of MS patients. Our results show that XBD173 at low dose decreases serum levels of pro-inflammatory interleukins, prevents the repression of myelin and axonal markers, and also ameliorates clinical deficits in EAE-PLP mice. The beneficial effect of XBD173 against clinical symptoms was also observed in the EAE-MOG mice mimicking the progressive MS. Promising perspectives are open for the development of effective strategies against MS with little or no serious side effects
Mohammadi, Behnam [Verfasser], and Christian [Akademischer Betreuer] Lohr. "Investigation of the therapeutic potential of the neuroprotective prion protein N1-fragment in cellular and mouse models of Alzheimers and prion disease / Behnam Mohammadi ; Betreuer: Christian Lohr." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2020. http://d-nb.info/1208394800/34.
Full textMohammadi, Behnam Verfasser], and Christian [Akademischer Betreuer] [Lohr. "Investigation of the therapeutic potential of the neuroprotective prion protein N1-fragment in cellular and mouse models of Alzheimers and prion disease / Behnam Mohammadi ; Betreuer: Christian Lohr." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2020. http://nbn-resolving.de/urn:nbn:de:gbv:18-103440.
Full textLai, Sau-wan, and 賴秀芸. "Investigating beta-amyloid peptide neurotoxicity from neuronal apoptosis to endoplasmic reticulum collapse: translational research back to basic science research." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B41633702.
Full textIsraelsson, Charlotte. "Molecular Characterization of Experimental Traumatic Brain Injury." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7087.
Full textArbo, Bruno Dutra. "Efeitos neuroprotetores do 4'-clorodiazepam em modelos experimentais de Doença de Alzheimer in vitro e sobre o desenvolvimento neuronal." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2016. http://hdl.handle.net/10183/147880.
Full textThe increase in life expectancy of the world population has been associated with a higher prevalence of neurodegenerative diseases. The Alzheimer’s Disease (AD) is the most common neurodegenerative disorder and the main cause of dementia among people over 60 years, being characterized by a progressive decline in the memory and mental function of the patients. These symptoms are associated with histopathological changes in the brain of these patients, including the presence of senile plaques, formed by the deposition of amyloid-beta (Aβ), and neurofibrillary tangles, which are related to the hyperphosphorylation of Tau protein. Studies indicate that Aβ deposition is a major contributor to AD progression, promoting neuronal damage through the activation of different pro-apoptotic pathways and giving rise to the typical dementia symptoms of this disease. To date, there are no effective treatments for AD, so that most of the pharmacological intervention is intended for the treatment of some of its symptoms. The translocator protein (TSPO) is located in contact sites between the outer and the inner mitochondrial membranes and is involved in the cholesterol transport into the mitochondria and in the regulation of steroidogenesis and apoptosis. Studies show that TSPO ligands present neuroprotective effects in different experimental models of brain injury and neurodegenerative diseases. Specifically regarding AD, a study indicated that 4’-chlorodiazepam (4’-CD), a TSPO ligand, is neuroprotective in an animal model of this disease, being a possible candidate for its treatment. Therefore, the aim of this study was to evaluate the neuroprotective effect of 4’-CD in different experimental models of Aβ- induced neurotoxicity in vitro, as well as its effects on the development of hipocampal neurons. First, it was demonstrated that 4’-CD decreased the cell death of SH-SY5Y cells exposed to the Aβ. This effect was associated with the inhibition of the Aβ-induced upregulation of Bax, a pro-apoptotic protein, and downregulation of survivin, a prosurvival protein. On the other hand, the expression of Bcl-xl and procaspase-3 was not change by the treatments. After, it was studied the neuroprotective effects of 4’-CD against Aβ in organotypic hipocampal cultures. In these experiments, it was shown that 4’-CD decreases the cell death of organotypic hippocampal slices exposed to the Aβ by increasing the protein expression of SOD, but without changing the expression of Akt and procaspase-3. Finally, due to the importance of the processes of neuronal development and maturation in the regeneration of CNS after injury, it was evaluated the effect of 4’-CD on the development of primary hippocampal neurons of male and female mice. It was observed that female primary hippocampal neurons presented an increased rate of development than male neurons. 4’-CD stimulated the development and increased the neuritic branching of male but not from female neurons. In summary, it was observed that 4’-CD presented a neuroprotective effect against Aβ in SH-SY5Y cells and in rat organotypical hippocampal slices, presenting itself as a promising agent for the treatment of AD. Also, it was observed that 4’-CD modulates the development of hippocampal neurons in a sex-dependent manner, stimulating the development of male but not from female cells.
Loureiro, Liliana Raquel Rodrigues. "DJ-1 mutants binding partners: insights into Parkinson's Disease." Master's thesis, Universidade de Aveiro, 2013. http://hdl.handle.net/10773/12583.
Full textParkinson´s disease (PD), the second most common progressive neurodegenerative disorder, is a multifactorial disease caused by both genetic and environmental factors. Among the genes associated with PD, DJ-1 is a multifunctional protein involved in oxidative stress response and neuroprotection. DJ-1 mutations, such as L166P, M26I and E163K lead to loss of protein function causing early onset autosomal recessive PD. Moreover, the residue C106 is considered crucial in DJ-1 function as a sensor of oxidative stress. In this study, one missense mutations (E163K) and two engineered mutations in the residue C106 (C106A and C106DD) were produced and characterized in order to evaluate the neuroprotective effect of each mutation and also characterize their dynamic interactome. Structural analysis confirmed the production of all the mutants in the dimeric form, with a molecular weight of approximately 43kDa. Moreover, protein´s thermal stability was assessed by thermal shift and the results showed that the mutant E163K was the less stable and the C106A the most stable. Secondary structure analysis was performed by circular dichroism and revealed similar secondary structures between DJ-1 WT and mutants. In addition, a LC-MS/MS was performed to determine proteins´ contaminants and the majority of the protein contaminants were coming from the expression system and culture medium used in proteins´ production. Moreover, neuroprotection assays revealed that DJ-1 WT did not protect SH-SY5Y cells under oxidative stress conditions. The dynamic interactome of DJ-1 WT and mutants C106DD, E163K and C106A was characterized under oxidative stress conditions. A wide number of binding partners were identified and for some of them quantification in the different conditions was also determined. These interactors have a broad range of functions but the majority are associated with cellular response to oxidative stress. The study of DJ-1 mutations is very important, since it gives elucidations into DJ-1 WT functions and related disease mechanisms. In this way, the putative DJ-1 WT interactors identified still lack validation, but from these characterized dynamic interactomes further elucidations can be obtained into Parkinson’s Disease pathology and potential new targets for PD prevention and therapy, like ATP-dependent RNA helicase DDX3X herein identified as new dynamic interactor of DJ-1.
A Doença de Parkinson, a segunda doença neurodegenerativa progressiva mais comum, é uma doença multifatorial causada conjuntamente por fatores genéticos e fatores ambientais. De entre os inúmeros genes associados à Doença de Parkinson, a DJ-1 é uma proteína multifuncional envolvida na resposta ao stress oxidativo e neuroproteção. Mutações na DJ-1, tais como L166P, M26I e E136K levam à perda de função da proteína causando a forma de Parkinson autossomal recessiva com desenvolvimento precoce. De salientar que o resíduo C106 é considerado crucial na função de sensor de stress oxidativo que a DJ-1 desempenha. Neste estudo, foram produzidas e caracterizadas duas mutações sintéticas no resíduo C106 (C106A e C106DD) e uma mutação natural (E163K) de modo a avaliar o efeito neuroprotetor de cada mutação bem como caracterizar o seu interactoma dinâmico. Análises estruturais confirmaram a produção de todos os mutantes na forma dimérica, apresentando um peso molecular de aproximadamente 43kDa. A estabilidade térmica das proteínas foi ainda avaliada por thermal shift e os resultados revelaram que o mutante E163K foi o menos estável enquanto que o mutante C106A foi o mais estável. Análise da estrutura secundária foi realizada por dicroísmo circular revelando elevada semelhança entre as estruturas secundárias da DJ-1 nativa e mutantes. Por fim, foi realizada uma análise de LC-MS/MS de modo a determinar os contaminantes das proteínas produzidas e verificou-se que a maioria dos contaminantes era proveniente do sistema de expressão e meio de cultura utilizados na produção das proteínas. Seguidamente, ensaios de neuroproteção revelaram que a DJ-1 nativa não exercia um efeito neuroprotetor nas células SH-SY5Y em condições de stress oxidativo. O interactoma dinâmico da DJ-1 nativa e mutantes C106DD, E163K e C106A foi caracterizado sob condições de stress oxidativo. Um elevado número de interactores foram identificados e para alguns deles foi possível obter uma quantificação nas diferentes condições. Os referidos interactores apresentam uma enorme variedade de funções, contudo a grande maioria está associada à resposta celular ao stress oxidativo. O estudo das mutações na DJ-1 é considerado muito relevante visto que fornece importantes elucidações relativamente às funções e mecanismos da DJ-1 nativa associados à doença. Neste sentido, os supostos interactores da DJ-1 nativa identificados ainda carecem de validação, mas da caracterização dos interactomas dinâmicos, elucidações podem ser obtidas sobre a patologia da Doença de Parkinson e identificação de novos potenciais alvos para prevenção e terapia desta doença, tal como a RNA helicase DDX3X dependente de ATP aqui identificada como novo interactor dinâmico da DJ-1.
Hobbs, Carey Anne. "Structural and functional characterization of bacterial response and neuroprotective proteins." 2009. http://www.lib.ncsu.edu/theses/available/etd-09082009-115433/unrestricted/etd.pdf.
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