Academic literature on the topic 'Maladie de Parkinson – Effets du stress'
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Journal articles on the topic "Maladie de Parkinson – Effets du stress":
Martel, Simon, Jonathan Y. Keow, and Marc Ekker. "Rotenone Neurotoxicity Causes Dopamine Neuron Loss in Zebrafish." University of Ottawa Journal of Medicine 5, no. 2 (November 2, 2015): 16–21. http://dx.doi.org/10.18192/uojm.v5i2.1413.
Jacquot, L. "Olfaction et troubles cognitifs. Application aux pathologies neurodégénératives." European Psychiatry 30, S2 (November 2015): S31. http://dx.doi.org/10.1016/j.eurpsy.2015.09.093.
Coulombe, Valérie, Léo Cantin, and Vincent Martel-Sauvageau. "Évaluation peropératoire de la parole dans la maladie de Parkinson." Psycause : revue scientifique étudiante de l'École de psychologie de l'Université Laval 8, no. 1 (September 5, 2019): 32–42. http://dx.doi.org/10.51656/psycause.v8i1.10111.
Jenner, Peter. "Maladie de Parkinson: m�canismes physiopathologiques et effets du pirib�dil." Journal of Neurology 240, S1 (1993): S2—S8. http://dx.doi.org/10.1007/bf00879099.
Hadjira, Sabrina, Bassim Bouchouf, Ahmed Menad, and Souad Ameddah. "Parkinson's disease, a neurodegenerative disorder that continues to be a challenge for scientific development." Batna Journal of Medical Sciences (BJMS) 8, no. 1 (June 4, 2021): 59–65. http://dx.doi.org/10.48087/bjmsra.2021.8111.
Gronchi-Perrin, Aline, and François Vingerhoets. "Effets cognitivo-comportementaux de la stimulation cérébrale profonde dans la maladie de Parkinson." Revue de neuropsychologie 1, no. 1 (2009): 59. http://dx.doi.org/10.3917/rne.011.0059.
Gronchi-Perrin, Aline, and François Vingerhoets. "Effets cognitivo-comportementaux de la stimulation cérébrale profonde dans la maladie de Parkinson." Revue de neuropsychologie Volume 1, no. 1 (March 1, 2009): 59–63. http://dx.doi.org/10.1684/nrp.2009.0008.
Michel-Flutot, Pauline, and Stéphane Vinit. "La stimulation magnétique répétée pour le traitement des traumas spinaux." médecine/sciences 38, no. 8-9 (August 2022): 679–85. http://dx.doi.org/10.1051/medsci/2022108.
Hammond, Constance. "La stimulation à haute fréquence dans la maladie de Parkinson : effets à court et long termes." médecine/sciences 21, no. 2 (February 2005): 127–28. http://dx.doi.org/10.1051/medsci/2005212127.
Ines, Bedoui, Linda Mrissa, Hajer Derbali, Anis Riahi, Mariem Messllemeni, J. Zaouali, and Malek Mansour. "Incrimination des facteurs de stress dans la survenue de maladie de Parkinson." Revue Neurologique 176 (September 2020): S92. http://dx.doi.org/10.1016/j.neurol.2020.01.266.
Dissertations / Theses on the topic "Maladie de Parkinson – Effets du stress":
Issa, Sabi Abdul-Raouf. "Stress oxydatif et vieillissement neuronal dans des modèles de la maladie de Parkinson chez la drosophile : effets protecteurs des protéines découplantes mitochondriales et de l'autophagie médiée par les chaperonnes." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066405.
Parkinson's disease (PD) is characterized by progressive motor disorders resulting in dopaminergic neurons degeneration in the substantia nigra. In this pathology, aging is a major predisposing factor. During my thesis, I examined initially, in vivo models used in the laboratory to study the PD in Drosophila, namely the expression of α-synuclein and paraquat. I have contributed to the identification of dopaminergic neurons subpopulation involved in locomotor effects of α-synuclein and highlighting the role of a dopamine D1-like receptor in neurotoxicity of paraquat. I then shown that the activity of dopaminergic neurons accelerated senescence and decreases Drosophila lifespan by contributing significantly to the production of ROS in the brain. Finally, we identified and characterized Drosophila homologous of LAMP-2A protein, involves in autophagy-mediated chaperone (AMC), and demonstrated that the increase in neuronal clearance of cytosolic proteins by the expression human LAMP-2A or its Drosophila homologue has positive effects on the locomotor decline associated with aging and resistance against PD factors, but it does not increase longevity. These results suggest that the CMA is a conserved mechanism in Drosophila and its activation protects against oxidative stress and neuronal aging
Besnault, Pierre. "Impact pathologique du stress chronique dans la maladie de Parkinson : rôle des récepteurs aux glucocorticoïdes dans la régulation des organelles de signalisation immunitaire innée." Electronic Thesis or Diss., Sorbonne université, 2023. http://www.theses.fr/2023SORUS534.
This project focuses on the pathological consequences of chronic stress (CS) and the alteration of signaling mediated by glucocorticoids (GCs) and their receptors (GRs) in Parkinson's disease (PD). Stress stimulates the hypothalamic-pituitary-adrenal (HPA) axis and the secretion of GCs that triggers a large number of physiological responses which are beneficial in the short term. On the other hand, CS disrupts the HPA axis, alters these physiological responses and leads to the development of neuropsychiatric disorders such as depression, a known risk factor for PD. In line with this, evidence suggests that the HPA axis is altered in PD patients together with a central alteration of GC/GR signaling. How could these alterations impact the pathomechanisms and contribute to disease progression? PD is an uncurable neurological disorder of still unknown origin. Sporadic form of the disease represents a very large majority of PD cases, and probably results from complex interactions between genetic and environmental risk factors. Clinically, PD is diagnosed upon identification of motor symptoms resulting from a massive loss of dopaminergic neurons in the substantia nigra. Neurodegeneration is associated with the aggregation of alpha-synuclein (aSyn) that deposits into intraneuronal inclusions known as Lewy bodies and neurites. Associated with neurodegeneration, immune responses orchestrating inflammatory processes are mounted and likely involved in disease progression. In the past years, one of the greatest finding regarding the mechanism of immune cell activation in PD has been the discovery of the structural properties of aSyn assemblies being able to act as true pathogen-associated molecular pattern, and to mediate the activation of supramolecular organizing centers (SMOCs), which are considered as important innate immune signaling platforms. Given that one of the major properties of GR is to regulate inflammatory response in immune cells, we hypothesize that chronic stress-mediated HPA axis and GC/GR signaling alterations could exacerbate inflammatory responses through an overactivation of SMOC-dependent signaling. Our work shows that CS not only alters microglial GC/GR signaling, but also increases neuronal death and microglia-associated inflammatory response in a mouse model of PD. Understanding precisely the link between the alteration of GC/GR signaling and the increase in the inflammatory response by focusing on SMOC-dependent signaling will allow us to better understand the different pathophysiological molecular mechanisms, but also identify new therapeutic targets
Levet, Clémence. "Mild Endoplasmic Reticulum Stress Protects From Cell Death : The Role Of Autophagy." Thesis, Lyon 1, 2012. http://www.theses.fr/2012LYO10209.
The last years have been very successful in identifying mechanisms, which control apoptosis in metazoan. However, the regulation of cell death in specific cell type remains to be determined. An excess of neuron apoptosis can lead to neurodegenerative diseases such as Huntington, Parkinson or Alzheimer diseases. Neurodegeneration is usually associated to Endoplasmic Reticulum stress (ER stress), autophagy or oxidative stress. However, the role of these mechanisms in the regulation of neurodegeneration is not clearly established. To test the role of ER stress in the regulation of neuronal death, we used several models of neurodegeneration in Drosophila and mammals. First, we have shown that the genetic induction of ER stress protected photoreceptors of the Drosophila eye from apoptosis. Then, we have shown that the protective effect of ER stress is conserved in both Drosophila and mouse models of Parkinson disease. In order to characterize the protective effect of ER stress, we have studied the activation of protective mechanisms upon ER stress. We have shown that in the Drosophila retina, ER stress can induce an anti-oxidative response and autophagy. Interestingly, autophagy is only activated in presence of both ER stress and cell death signal. We have focused on the role of autophagy in the protective effect of ER stress. We have shown that the activation of autophagy was required for the protective effect of ER stress. Thus, we have shown that ER stress response is not only involved in the reduction of misfolded protein accumulation, but can also protect neurons form cell death by activating autophagy
Séré, Yves Yacouba. "Effet de la biosynthèse de lipides sur la toxicité de l'α-synucléine, protéine impliquée dans la maladie de Parkinson, chez Saccharomyces cerevisiae." Poitiers, 2010. http://theses.edel.univ-poitiers.fr/theses/2010/Sere-Yves-Yacouba/2010-Sere-Yves-Yacouba-These.pdf.
Parkinson’s disease is a neurodegenerative pathology that has been linked to several genetic mutations of the SNCA gene encoding the pro-oxidant α-synuclein protein. The budding yeast S. Cerevisiae is a valuable model to study cellular and molecular mechanisms of α-synuclein toxicity. Indeed heterologous expression of α-synuclein is toxic to wild type yeast, and recapitulates the main features of damages caused to mammalian neurons including an increase of neutral lipids storage (triglycerides and steryl esters, embedded into lipid droplets). To address the significance of this accumulation, we forced α-synuclein production in a strain unable to synthesize triglycerides and steryl esters. Surprisingly, inability to store neutral lipids rendered cells more tolerant to α-synuclein. Our results indicate that the level of !-synuclein toxicity is correlated to fatty acid synthase activity and intracellular redox state
Rahbari, Oskoui Farid. "Stress oxydatif, vieillissement et maladie de Parkinson." Bordeaux 2, 1997. http://www.theses.fr/1997BOR2M024.
Lefeuvre, Jocelyne. "Dépression, Dopamine et maladie de Parkinson." Bordeaux 2, 1991. http://www.theses.fr/1991BOR23034.
Laplace, Martine. "Radicaux libres et maladie de Parkinson." Bordeaux 2, 1996. http://www.theses.fr/1996BOR2P017.
Jourdes, Peggy. "Électrotransfert de gènes et effets du néovastat(R) dans les glioblastomes : approche pré-clinique de deux traitements de pathologies cérébrales." Université Joseph Fourier (Grenoble), 2002. http://www.theses.fr/2002GRE19012.
The treatment of neurodegenerative diseases and glioblastoma requires the development of new therapies such as gene therapy or new molecules synthesis. The transfection of central nervous system (CNS) cells or muscular cells aims to allow the expression in the long term of favorable factors for the etiologic treatment of the disease. We optimized the parameters of electrotranfer in the mice muscle (5*900V , 99æs, 1 Hz) and in the brain of mice and rats (10*600V, 99æs, 1Hz). The electrotransfer increases by 500 the rate of transgene in the muscle and by 700 to 1000 in the CNS. The voltages seem to be far from the applicable parameters in high frequency deep brain stimulation in Parkinson's disease. We revised the methodology applied with low frequency and we demonstrated the transfection of the rat CNS by high frequency stimulation (130 Hz) with a current intensity of 3 mA and a pulse width of 99 æs. So, we get closer to clinical parameters. As regards the treatment of the malignant glioblastoma, no conventional therapy turned out to be effective. The elaboration of Neovastatâ by Aeterna laboratories presents promising preclinical results. Indeed, this medicine which consists of active factors issued from the shark cartilage, is a natural antiangiogenic and antitumoror agent that possesses an important therapeutic potential
Souchay, Céline. "Exploration de la métamémoire dans le vieillissement normal, la maladie d'Alzheimer et la maladie de Parkinson." Tours, 2000. http://www.theses.fr/2000TOUR2019.
Jourdain, Vincent. "Effets de la neurostimulation dans la douleur chronique et la maladie de Parkinson." Thesis, Université Laval, 2010. http://www.theses.ulaval.ca/2010/27883/27883.pdf.
Books on the topic "Maladie de Parkinson – Effets du stress":
National Parkinson Foundation Symposium on Parkinson Research (1st 1988 Miami Beach, Fla.). Progress in Parkinson research. New York: Plenum Press, 1988.
Hefti, Franz, and William J. Weiner. Progress in Parkinson Research. Springer, 1989.
Hefti, Franz, and William J. Weiner. Progress in Parkinson Research. Springer, 2011.
Hefti, Franz. Progress in Parkinson Research. Springer, 2011.