Dissertationen zum Thema „Mitochondrial movement“
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Shchepinova, Maria M. „Molecular probes for monitoring mitochondrial movement and function“. Thesis, University of Glasgow, 2016. http://theses.gla.ac.uk/7835/.
Der volle Inhalt der QuelleVaillant-Beuchot, Loan. „Étude des mécanismes liés aux dysfonctions mitochondriales, à l'altération de la mitophagie et aux défauts du transport mitochondrial dans la maladie d'Alzheimer“. Electronic Thesis or Diss., Université Côte d'Azur, 2022. http://www.theses.fr/2022COAZ6019.
Der volle Inhalt der QuelleMitochondria are essential organelles in cells, ensuring energy production with ATP synthesis, calcium buffering, apoptosis regulation. These functions are altered at early stages of Alzheimer's disease (AD) and are essentially induced by the Amyloid (Aβ), produced after the sequential cleavage of amyloid precursor protein (APP) by β- and γ-secretase. Aβ is a major actor of AD development but all the treatments targeting this peptide remain ineffective. C-terminal APP fragments (APP-CTFs: C83 and C99 (Aβ precursor) are other fragments presenting specific toxicity in AD and new potential therapeutic targets. My project is focus on the study of APP-CTFs toxicity, independently of Aβ, on the structure, function of mitochondria, their degradation by mitophagy and on mitochondrial transport proteins. They constitute the complex allowing mitochondrial transport in cells, especially in neurons, closely linked to mitochondrial renewal, particularly in neurons.First axe: APP-CTFs impact on mitochondrial structure, function and mitophagy. We described APP-CTFs accumulation in mitochondrial fraction in vitro (human neuroblastoma cells expressing APP Swedish double mutation (SH-SY5Y-APPswe) or C99 fragment (SH-SY5Y-C99)) and in vivo (3xTgAD mice expressing APPswe, TauP301L, PS1 (M146V) or C99 fragment after viral injection). We inhibit the cleavage of APP-CTFs and the production of Aβ by pharmacological approaches, to abolish γ-secretase activity. Ours results show for the first time in vitro and in vivo, that high concentration of APP-CTFs independently of Aβ, impact mitochondrial structure, function and alter mitophagy process, resulting in an accumulation of altered mitochondria producing high levels of toxic reactive oxygen species. In addition, our results in patient brains of sporadic AD (SAD) patients show altered mitophagic protein levels correlating with APP-CTFs accumulation (1-2).Second axe: study of the effects of APP, APP-CTFs and Aβ peptide on mitochondrial transport machinery. I reported the specific regulation of mitochondrial transport protein by endogenous APP (Mice fibroblasts APP WT and KO) and the overexpression of APPswe (and in SH-SY-5Y-APPswe cells). APP-CTFs and Aβ differentially regulate mitochondrial transport protein levels in treated SH-SY-5Y-APPswe cells with γ-secretase inhibitor. These results were validated in mice fibroblasts KO for presenilins (catalytic compounds of γ-secretase) avoiding APP-CTFs degradation. APP-CTFs and Aβ impair the recruitment of mitochondria to its transport machinery in differentiated SHSY-5Y. The progression of the disease deregulates the levels of mitochondrial transport protein in vivo (3xTgAD and WT mice brains, C99 injected mice brains) and in SAD patients brains. The analyses of young and old mice brains and of SAD patients samples at different stages of the disease, allowed us to demonstrate an impact of aging in the regulation of mitochondrial transport protein levels. This phenomenon occurs also in addition with AD progression (3).These studies highlight new molecular mechanisms impacting mitochondrial homeostasis during AD progression. Our findings will bring new therapeutic research to slow down mitochondrial dysfunctions and/or to stimulate their renewal in AD context.(1). Vaillant-Beuchot L.*, Mary A.* et al. Acta Neuropathologica 2020.(2). Mary A.*, Vaillant-Beuchot L.* et al. Médecine/sciences 2021.(3). Vaillant-Beuchot et al. En cours de soumission
Eshleman, Jason Aaron. „Mitochondrial DNA and prehistoric population movements in western North America /“. For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2002. http://uclibs.org/PID/11984.
Der volle Inhalt der QuelleMurphy, Cheryl. „Influence of post-aerobic exercise nutrition on protein turnover and mitochondrial biogenesis“. 2009. http://hdl.handle.net/2292/5429.
Der volle Inhalt der QuelleGranata, Cesare. „Effects of different exercise intensity and volume on markers of mitochondrial biogenesis in human skeletal muscle“. Thesis, 2015. https://vuir.vu.edu.au/30176/.
Der volle Inhalt der QuelleWang, Xiao Nan. „Skeletal muscle mitochondrial capacity and metabolism in lung transplant patients and resistance trained subjects“. Thesis, 2000. https://vuir.vu.edu.au/15725/.
Der volle Inhalt der QuelleHedges, Christopher. „The effects of physiological acidosis on skeletal muscle mitochondrial function, ROS balance, and intracellular signalling“. Thesis, 2017. https://vuir.vu.edu.au/35976/.
Der volle Inhalt der QuelleJamnick, Nicholas. „An examination of current methods to prescribe exercise intensity: validity of different approaches and effects on cell signalling events associated with mitochondrial biogenesis“. Thesis, 2019. https://vuir.vu.edu.au/40459/.
Der volle Inhalt der QuelleBartlett, Jonathan. „Exercise-induced cell signalling responses of human skeletal muscle: the effects of reduced carbohydrate availability“. Thesis, 2012. https://vuir.vu.edu.au/29596/.
Der volle Inhalt der QuelleWoessner, Mary. „BEET-HF: The Effects of Dietary Inorganic Nitrate Supplementation on Aerobic Exercise Performance, Vascular Function, Cardiac Performance and Mitochondrial Respiration in Patients with Heart Failure with Reduced Ejection Fraction“. Thesis, 2019. https://vuir.vu.edu.au/40041/.
Der volle Inhalt der QuelleSerpiello, Fabio. „Intermittent-sprint exercise: performance and muscle adaptations in health and chronic disease“. Thesis, 2012. https://vuir.vu.edu.au/34681/.
Der volle Inhalt der QuelleSaner, Nicholas. „Can exercise mitigate the negative metabolic effects associated with sleep loss?“ Thesis, 2019. https://vuir.vu.edu.au/40011/.
Der volle Inhalt der QuellePapadimitriou, Ioannis D. „The influence of ACTN3 R577X genotype on performance and muscle adaptations to a single bout of exercise“. Thesis, 2018. https://vuir.vu.edu.au/37829/.
Der volle Inhalt der QuelleHill, Karen M. „How do different dietary dairy proteins, ingested post-exercise, effect adaptations to endurance training?“ Thesis, 2017. https://vuir.vu.edu.au/40588/.
Der volle Inhalt der QuellePierson, Melanie. „Deciphering the mtDNA record of prehistoric population movements in Oceania : a thesis submitted in partial fulfilment of the requirements for the degree of Doctor of Philosophy in Zoology, University of Canterbury /“. 2007. http://library.canterbury.ac.nz/etd/adt-NZCU20080331.135504.
Der volle Inhalt der QuelleKjertakov, Metodija. „The role of heat as a conditioning stimulus in endurance athletes“. Thesis, 2019. https://vuir.vu.edu.au/40031/.
Der volle Inhalt der QuelleSmith, Graeme. „Dietary and exercise manipulation of skeletal muscle function in older humans“. Thesis, 2010. https://vuir.vu.edu.au/16011/.
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