Dissertations / Theses on the topic 'Nervous system – Degeneration'
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Biro, Andrew J. "Specific aspects of neurodegenerative disease." Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/28919.
Full textMedicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate
Babetto, Elisabetta. "Axon degeneration mechanisms in Alzheimer's disease and injury." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609249.
Full textGodzik, Katharina. "The NAD salvage pathway and Wallerian degeneration." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.707906.
Full textTsao, Jack W. "Wallerian degeneration in normal mice and in mutant C57BL/Wld mice." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260174.
Full textLunn, Elizabeth Ruth. "Studies on the degeneration and regeneration of neurons to skeletal muscle." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.292675.
Full textHung, Hiu-ling, and 洪曉翎. "Characterization of mitochondrial morphology and dynamics in neurodegeneration." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B50126362.
Full textDuan, Rui-Sheng. "Inflammation and neurodegeneration in mouse nervous system: experimental application /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-606-9/.
Full textMaharaj, Deepa Sukhdev. "An investigation into the physico-chemical and neuroprotective properties of melatonin and 6-hydroxymelatonin." Thesis, Rhodes University, 2003. http://eprints.ru.ac.za/71/.
Full textSchwarz, Stefan Theodor. "Magnetic resonance imaging correlates of neuronal degeneration of brain stem nuclei in Parkinson's disease." Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/37023/.
Full textHughes, P. M. "Role of matrix metalloproteinases in inflammatory demyelination of the peripheral nervous system." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390492.
Full textChan, Pok-man. "Cloning of hamster GAP-43 to study the expression and regulation of GAP-43 mRNA in the retina during degeneration and regeneration /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B2063299X.
Full textSu, Huanxing. "Transplantation of neural stem cells for motoneuron degeneration due to axonal injury." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41290537.
Full textMoore, Leah Kathryn. "Neuronal viability and biochemical alterations after mechanical stretch injury: ban in vitro model of traumatic brain injury-induced neourodegeneration." Thesis, Georgia Institute of Technology, 2003. http://hdl.handle.net/1853/5362.
Full textCullen, Daniel Kacy. "Traumatically-induced degeneration and reactive astrogliosis in three-dimensional neural co-cultures." Available online, Georgia Institute of Technology, 2005, 2005. http://etd.gatech.edu/theses/available/etd-11282005-210117/.
Full textRobert McKeon, Committee Member ; Robert Lee, Committee Member ; Robert Guldberg, Committee Member ; Ravi Bellamkonda, Committee Member ; Michelle LaPlaca, Committee Chair. Vita.
Ho, Wing-lau, and 何穎流. "Investigating neurodegeneration in the retina of tau P301L mice." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B4833392X.
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Anatomy
Master
Master of Medical Sciences
麥超常 and Chiu-sheung Simon Mak. "Efficacy of herbal medicine on neurodegenerative diseases: a systematic review." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40738905.
Full textGong, Nanjie, and 龔南杰. "Probing tissue microstructural changes in neurodegenerative processes using non-gaussian diffusion MR imaging." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/208583.
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Diagnostic Radiology
Doctoral
Doctor of Philosophy
Kadanthode, Rubina John. "An investigation into the neuroprotective effects of melatonin in a model of rotenone-induced neurodegeneration." Thesis, Rhodes University, 2004. http://hdl.handle.net/10962/d1003241.
Full textHeron, Paula Michelle. "An investigation of the neuroprotective effects of estrogen in a model of quinolinic acid-induced neurodegeneration." Thesis, Rhodes University, 2002. http://hdl.handle.net/10962/d1003237.
Full textParmar, Paresh H. "An investigation into the possible neuroprotective role of melatonin in copper-loading." Thesis, Rhodes University, 2001. http://hdl.handle.net/10962/d1003261.
Full textGeorgiou, A. L. "The consequences for central nervous system synaptic transmission following retinal degeneration and its treatment." Thesis, University College London (University of London), 2009. http://discovery.ucl.ac.uk/18910/.
Full text周智豪 and Chi-ho Chau. "Neural glycosaminoglycans and their effects on post-traumatic regrowthof sciatic nerves in adult guinea pigs." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31236625.
Full textEdwards, Malia Michelle 1975. "Alteration of astrocyte-specific protein expression : implications for Alzheimer's disease." Monash University, Dept. of Psychology, 2002. http://arrow.monash.edu.au/hdl/1959.1/7859.
Full textViar, Kenneth E. II. "Role of SARM1 in Chronic Immune-Mediated Central Nervous System Inflammation." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5819.
Full textSu, Huanxing, and 蘇煥興. "Transplantation of neural stem cells for motoneuron degeneration due to axonal injury." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41290537.
Full text陳博文。 and Pok-man Chan. "Cloning of hamster GAP-43 to study the expression and regulation of GAP-43 mRNA in the retina during degeneration and regeneration." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31220423.
Full textSchofield, Emma Medical Sciences Faculty of Medicine UNSW. "Characterisation of cortical pathology and clinicopathological correlates in progressive supranuclear palsy." Awarded by:University of New South Wales. School of Medical Sciences, 2006. http://handle.unsw.edu.au/1959.4/27326.
Full textJoshi, Priyanka. "Targeting intrinsically disordered proteins associated with neurodegenerative diseases : a strategy towards drug discovery." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709234.
Full textHuseynova, Gunel. "Novel autophagy regulators that affect polyglutamine pathology in Drosophila." Thesis, University of Cambridge, 2016. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709531.
Full textChoi, Minee. "Adult neurogenesis and dopamine in neurodegenerative diseases." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607778.
Full textDaniel, Sheril. "An investigation into the neuroprotective properties of curcumin." Thesis, Rhodes University, 2003. http://hdl.handle.net/10962/d1003231.
Full textShi, Ri Yi. "Neuronal Survival After Dendrite Amputation: Investigation of Injury Current Blockage." Thesis, University of North Texas, 1988. https://digital.library.unt.edu/ark:/67531/metadc501278/.
Full textRavula, Surendra Kumar. "A Multielectrode Microcompartment Platform for Signal Transduction in the Nervous System." Diss., Georgia Institute of Technology, 2006. http://hdl.handle.net/1853/11527.
Full textRooney, Timothy M. "Genes Required for Wallerian Degeneration Also Govern Dendrite Degeneration: A Dissertation." eScholarship@UMMS, 2015. https://escholarship.umassmed.edu/gsbs_diss/775.
Full textRooney, Timothy M. "Genes Required for Wallerian Degeneration Also Govern Dendrite Degeneration: A Dissertation." eScholarship@UMMS, 2004. http://escholarship.umassmed.edu/gsbs_diss/775.
Full textChen, Yongmei. "Excitotoxicity in neurodegenerative disorders." free to MU campus, to others for purchase, 1998. http://wwwlib.umi.com/cr/mo/fullcit?p9901225.
Full textLi, Yan, and n/a. "In vitro and in vivo studies on the absorption of mitoquinone." University of Otago. School of Pharmacy, 2007. http://adt.otago.ac.nz./public/adt-NZDU20070615.135534.
Full textWuwongse, Suthicha. "Investigation of synaptic degeneration as a common culprit underlying the neurodegenerative process induced by corticosterone and beta-amyloid." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B49617874.
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Psychiatry
Doctoral
Doctor of Philosophy
Haylett, William Lloyd. "Identification of parkin interactions: implications for Parkinson’s disease." Thesis, Stellenbosch : Stellenbosch University, 2015. http://hdl.handle.net/10019.1/97854.
Full textENGLISH ABSTRACT: Parkinson’s disease (PD) is a progressive and debilitating neurodegenerative disorder, characterized by a distinct motor phenotype and the selective loss of dopaminergic neurons in the substantia nigra. While the etiology of PD is not fully understood, it is thought to involve a combination of different genetic, cellular and environmental factors that independently or concurrently contribute to neurodegeneration. To date, several PD-causing genes have been identified, and investigations of their function have provided novel insights into the pathobiology of disease. Particularly interesting among the known PD genes is parkin, mutations in which are the most common genetic cause of early onset PD. Parkin is an E3 ligase that ubiquitinates protein substrates and targets such substrates for degradation via the ubiquitin proteasome system (UPS). Therefore, the loss of parkin may result in the deleterious accumulation or dysregulation of parkin substrates and neurotoxicity. Parkin’s enzymatic activity has also been implicated in the maintenance of mitochondrial health, and mitochondrial dysfunction is commonly reported in cellular and animal models of parkin deficiency. This study aimed to investigate parkin and its role in PD on various levels. Initially, genetic screening approaches were used to assess the contribution of parkin mutations to PD in a group of 229 South African patients. It was concluded that parkin mutations are rare in the South African PD population, being present in only seven (3.1%) patients in the study group. Interestingly, this study identified two of only three Black African PD patients with mutations in a known PD-causing gene to date. The low frequency of known PD genes raises the interesting possibility that the unique South African ethnic groups may harbor mutations in novel PD-causing genes. Although many parkin-interacting proteins have been identified in the literature, it is anticipated that novel, pathologically-relevant parkin substrates remain to be discovered. Hence, this study used a yeast two-hybrid (Y2H) approach to identify novel parkin interactions. This yielded 29 putative parkin interactors, of which four, namely ATPAF1, SEPT9, actin and 14-3-3η, were prioritized for verification by co-localization and co-immunoprecipitation experiments. Interestingly, two of the parkin interactors (ATPAF1 and SEPT9) were found to accumulate in the absence of parkin, supporting their role as authentic parkin substrates. The identification of these two intriguing proteins implicates parkin in the regulation of mitochondrial ATP synthase assembly and septin filament dynamics, which may be of significant relevance to our understanding of processes underlying neurodegeneration. Moreover, it was aimed to assess various markers of mitochondrial function in a parkin-deficient cellular model, as previous studies had reported conflicting results regarding mitochondrial impairments in patient-derived cells with parkin mutations. Hence, dermal fibroblasts were obtained from PD patients with homozygous parkin mutations, after which cell growth and viability, mitochondrial membrane potential, respiratory rates and the integrity of the mitochondrial network were assessed. Surprisingly, it was found that cell growth was significantly higher in the parkin-mutant fibroblasts compared to wild-type controls fibroblasts under basal conditions (p=0.0001), while exhibiting a greater inhibition of cell growth in the presence of the mitochondrial toxin CCCP (p=0.0013). Furthermore, whereas the mitochondrial networks of patient-derived fibroblasts were more fragmented than controls (p=0.0306), it was found that mitochondrial respiratory rates were paradoxically higher in the patients (p=0.0355). These unanticipated findings are suggestive of a compensatory response to the absence of parkin. The parkin-deficient cellular model was also used in a pilot study of the functional effects of vitamin K2 treatment, which has recently been identified as a promising PD therapeutic modality. It was found that treatment with vitamin K2 resulted in more interconnected mitochondrial networks (p=0.0001) and enhanced respiratory rates (p=0.0459) in both parkin-mutant and wild-type control cells. While these results need to be studied further, it suggests that vitamin K2 supplementation may be of use as a general promoter of mitochondrial integrity and function. In conclusion, this dissertation highlights some novel interactions of the parkin protein and some interesting phenotypes of parkin deficiency. It is hoped that further investigation of parkin and its role in PD will, ultimately, aid in the development of therapeutic strategies to treat this debilitating and poorly-understood disorder.
AFRIKAANSE OPSOMMING: Parkinson se siekte (PS) is 'n progressiewe en aftakelende neurodegeneratiewe kondisie, wat gekarakteriseer word deur 'n kenmerkende bewegingsfenotipe en die selektiewe afsterwing van dopaminergiese neurone in die substantia nigra. Terwyl die etiologie van PS nie ten volle verstaan is nie, behels dit waarskynlik 'n kombinasie van verskillende genetiese, sellulêre en omgewings-faktore wat onafhanklik of gelyktydig lei tot senuwee-afsterwing. Tot op hede is daar al verskeie PS-veroorsakende gene geïdentifiseer, en die bestudering van hul funksie het nuwe insigte in die patobiologie van hierdie siekte verskaf. Onder meer hierdie PS gene is parkin van besondere belang, aangesien mutasies in parkin die mees algemene genetiese oorsaak van vroeë-aanvang PS is. Parkin is 'n E3 ligase-ensiem wat proteïen substrate ubiquitineer en teiken vir degradasie via die ubiquitien proteasoomstelsel (UPS). Dus kan die verlies van parkin lei tot die beskadigende opeenhoping of wanregulasie van parkin substrate en senuwee-afsterwing. Parkin se ensiematiese aktiwiteit is ook betrokke by die instandhouding van mitokondriale gesondheid, en mitokondriale afwykings word dikwels gerapporteer in sellulêre en diermodelle van parkin tekort. Hierdie studie het gepoog om parkin en sy rol in PS op verskillende vlakke te ondersoek. Aanvanklik is genetiese siftingsbenaderinge gebruik om die bydrae van parkin mutasies tot PS in 'n groep van 229 Suid-Afrikaanse pasiënte te evalueer. Die gevolgtrekking is bereik dat parkin mutasies skaars is in die Suid-Afrikaanse PS bevolking, aangesien dit teenwoordig is in net sewe (3.1%) pasiënte in die studie groep. Interessant genoeg, hierdie studie het twee van slegs drie gevalle van Swart Afrika-pasiënte met mutasies in 'n bekende PS geen to op datum geïdentifiseer. Die lae frekwensie van bekende PS gene versterk die stimulerende moontlikheid dat die unieke Suid-Afrikaanse sub-populasies dalk mutasies in nuwe PS-veroorsakende gene mag koester. Alhoewel baie parkin proteïen-interaksies reeds in die literatuur geïdentifiseer is, word daar verwag dat nuwe, patologies-relevante parkin substrate nog wag om ontdek te word. Dus het hierdie studie 'n gis twee-hibried (G2H) benadering gebruik om nuwe parkin interaksies te identifiseer. Hierdie het 29 vermeende parkin interaktors opgelewer, waarvan vier, naamlik ATPAF1, SEPT9, aktien en 14-3-3η, geprioritiseer is vir verifikasie deur mede-lokalisering en mede-immunopresipitasie eksperimente. Interessant genoeg, daar is gevind dat twee van die parkin interaktors (ATPAF1 en SEPT9) ophoop in die afwesigheid van parkin, wat hul rol as werklike parkin substrate ondersteun. Die identifisering van hierdie twee interessante proteïene impliseer parkin in die regulering van mitokondriale ATP sintase vervaardiging en septienfilament dinamika, wat moontlik van beduidende belang is vir ons begrip van die onderliggende prosesse wat senuwee-afsterwing veroorsaak. Verder is daar daarop gemik om verskeie aanwysigings van mitokondriale funksie in 'n parkin-gebrekkige sellulêre model te evalueer, aangesien vorige studies teenstrydige resultate rapporteer rakende mitokondriale afwykings in pasiënt-selle met parkin mutasies. Dus is daar dermale fibroblaste verkry van PS pasiënte met homosigotiese parkin mutasies, waarna sel-groei en lewensvatbaarheid, mitokondriale membraanpotensiaal, respiratoriese tempo en die integriteit van die mitokondriale netwerk geëvalueer is. Daar is verbasend gevind dat sel-groei aansienlik hoër is die parkin-mutante fibroblaste in vergelyking met wilde-tipe kontrole fibroblaste onder basale kondisies (p=0.0001), terwyl hulle 'n groter inhibisie van sel-groei in die teenwoordigheid van die mitokondriale toksien CCCP ondergaan (p=0.0013). Verder, terwyl die mitokondriale netwerke van pasiënt fibroblaste meer gefragmenteer is as die van kontroles (p=0.0306), is daar gevind dat mitokondriale respiratoriese tempo’s, paradoksaal-gewys, hoër is in die pasiënte (p=0.0355). Hierdie onverwagte bevindinge is suggestief van die aanskakeling van 'n vergoedende respons-proses in die afwesigheid van parkin. Die parkin-gebrekkige sellulêre model is ook gebruik in 'n voorlopige studie van die funksionele effekte van vitamiene K2 behandeling, wat onlangs geïdentifiseer is as 'n belowende terapeutiese moontlikheid vir PS. Daar is gevind dat sel-behandeling met vitamiene K2 lei tot meer geïnterkonnekteerde mitokondriale netwerke (p=0.0001) en verbeterde respiratoriese fuksie (p=0.0459) in beide parkin-mutante en wilde-tipe kontrole selle. Terwyl hierdie resultate verder bestudeer sal moet word, dui dit daarop dat vitamiene K2-aanvulling moontlik gebruik kan word as 'n algehele promotor van mitochondriale integriteit en funksie. Ten slotte, hierdie verhandeling beklemtoon ‘n paar nuwe interaksies van die parkin proteïen en 'n paar interessante fenotipes van parkin tekort. Daar word gehoop dat verdere ondersoek van parkin en parkin se rol in PS sal, uiteindelik, steun in die ontwikkeling van terapeutiese strategieë om hierdie aftakelende en swak-verstaande wanorde beter te behandel.
Liu, Xiaoying. "Pattern of synapse loss in neurodegenerative disorders a comparison between frontal lobe degeneration of non-Alzheimer type and Alzheimer's disease /." Lund : Dept. of Neuropathology, Institute of Pathology, Lund University, 1995. http://catalog.hathitrust.org/api/volumes/oclc/39783697.html.
Full textPan, Tao. "Genetic and physical interaction of Sgt2 protein with prion-chaperone machinery." Thesis, Georgia Institute of Technology, 2011. http://hdl.handle.net/1853/45765.
Full textClarkson, Andrew N., and n/a. "Lasting neuroprotection with clomethiazole following hypoxia-ischaemia-induced neurodegeneration : a mechanistic study." University of Otago. Department of Pharmacology & Toxicology, 2005. http://adt.otago.ac.nz./public/adt-NZDU20070424.120005.
Full textFok, Lai-chun, and 霍麗珍. "Neuroprotection of retinal ganglion cells with laser therapy." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31969616.
Full textChao, Jianfei, and 巢剑非. "Effects of resveratrol derivatives in preventing neurodegeneration of Parkinson's disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45553774.
Full textChua, Ka Kit. "Randomized controlled clinical trials for the evaluation of efficacy and safety of Chinese medicine in treatment of neurodegenerative diseases." HKBU Institutional Repository, 2015. https://repository.hkbu.edu.hk/etd_oa/231.
Full textCheung, Hiu-yee Zelda, and 張曉宜. "Neuroprotection by a mixture of herbal extracts following axotomy: its effect on the molecular mechanisms ofaxotomized retinal ganglion cell death." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31242984.
Full textWang, Ziying. "Neuroprotective effects of a novel TFEB activator E4 and its self-carried nanoparticles in MPTP-induced Parkinson's disease models." HKBU Institutional Repository, 2019. https://repository.hkbu.edu.hk/etd_oa/695.
Full textRamsunder, Adrusha. "An investigation into the possible neuroprotective or neurotoxic properties of metrifonate." Thesis, Rhodes University, 2005. http://hdl.handle.net/10962/d1007560.
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Tan, Yuan. "Using induced pluripotent stem cells to establish disease models with neurodegenerative disorders." Thesis, University of Macau, 2018. http://umaclib3.umac.mo/record=b3952490.
Full textCaprariello, Andrew Vincent. "Cytoarchitectural Defects Secondary To Experimentally Induced Oligodendrocyte Death In The Adult And Developing Central Nervous System." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1346859526.
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