Literatura académica sobre el tema "Modélisation des maladies neurodégénératives"
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Artículos de revistas sobre el tema "Modélisation des maladies neurodégénératives"
Lautier, Corinne y Florin Grigorescu. "Maladies neurodégénératives et diabète". médecine/sciences 25, n.º 4 (abril de 2009): 337–40. http://dx.doi.org/10.1051/medsci/2009254337.
Texto completoMarin, Benoît y Maëlenn Guerchet. "Ethnicité et maladies neurodégénératives". Revue Neurologique 173 (marzo de 2017): S196—S197. http://dx.doi.org/10.1016/j.neurol.2017.01.388.
Texto completoKontush, A. y M. J. Chapman. "HDL et maladies neurodégénératives". Médecine des Maladies Métaboliques 3, n.º 1 (enero de 2009): 43–47. http://dx.doi.org/10.1016/s1957-2557(09)70103-8.
Texto completoGuillet-Pichon, V. y C. Verny. "Mitochondrie et maladies neurodégénératives". Pratique Neurologique - FMC 7, n.º 2 (abril de 2016): 117–22. http://dx.doi.org/10.1016/j.praneu.2016.01.024.
Texto completoGiménez y Ribotta, Minerva y Alain Privat. "Maladies neurodégénératives : thérapie génique". Annales de l'Institut Pasteur / Actualités 11, n.º 2 (abril de 2000): 79–96. http://dx.doi.org/10.1016/s0924-4204(00)80012-8.
Texto completoGiménez y Ribotta, Minerva y Alain Privat. "Maladies neurodégénératives : thérapie génique". Journal of Engineering and Technology Management 14, n.º 2 (junio de 1997): 79–96. http://dx.doi.org/10.1016/s0923-4748(97)80012-4.
Texto completoBurkhard, Pierre, François Vingerhoets, Julien Bogousslavsky y Theodor Landis. "Revisiter les maladies neurodégénératives". Revue Médicale Suisse 2, n.º 64 (2006): 1147–48. http://dx.doi.org/10.53738/revmed.2006.2.64.1147.
Texto completoStevanin, Giovanni. "Transport axonal et maladies neurodégénératives". Neurologie.com 1, n.º 3 (mayo de 2009): 066–67. http://dx.doi.org/10.1684/nro.2008.0031.
Texto completoEmile, Carole. "Marqueurs biologiques des maladies neurodégénératives". Option/Bio 30, n.º 591-592 (enero de 2019): 26–28. http://dx.doi.org/10.1016/s0992-5945(19)30008-x.
Texto completoDauvilliers, Y. "Insomnie dans les maladies neurodégénératives". Revue Neurologique 163, n.º 4 (abril de 2007): 237–38. http://dx.doi.org/10.1016/s0035-3787(07)90947-9.
Texto completoTesis sobre el tema "Modélisation des maladies neurodégénératives"
Lemonnier, Thomas. "Modélisation de maladies neurodégénératives à l’aide de cellules souches pluripotentes induites humaines". Thesis, Paris 5, 2012. http://www.theses.fr/2012PA05T074/document.
Texto completoReprogramming technology of somatic cells in induced pluripotent stem cells (iPS) now offers the opportunity to model neurodegenerative diseases and to study patient’s neurons. We used this technology for generating two models of neurodegenerative diseases: the muccopolysaccharidosis type IIIB (MPSIIIB) and the ALS2 form of amyotrophic lateral sclerosis (ALS). In the MPSIIIB model, we have shown that iPS and neurons of patients had characteristic defects of the disease such as the accumulation of storage vesicles. Alterations of the Golgi apparatus in these cells were also highlighted. Transcriptome analysis of MPSIIIB neural precursors showed transcriptional changes involving particularly genes implicated in cell-extracellular matrix interactions. Thus, in a subsequent study, alterations of migration and orientation of MPSIIIB mutant mouse cells and MPSIIIB patients’ cells have been demonstrated. These alterations may be responsible for the disruption of neurogenesis and neuritogenesis in sick children. In the ALS2 model, we have shown that patients’ neurons had defects including decreased endosomes’ surface and abnormal neurite outgrowth. As there was previously no relevant cellular model reproducing the disease, this model will now allow the study of physiopathological processes involved in the disease. In conclusion, the generation of iPS cells allows to model neurodegenerative diseases and to study associated physiopathological processes on cultured human neurons. These cell models could allow in the near future the screening of molecules of potential therapeutical interest
Lemonnier, Thomas. "Modélisation de maladies neurodégénératives à l'aide de cellules souches pluripotentes induites humaines". Phd thesis, Université René Descartes - Paris V, 2012. http://tel.archives-ouvertes.fr/tel-00806699.
Texto completoHaffaf, Hadjer Wafaa. "Analyse de l'agrégation des protéines dans les maladies neurodégénératives amyloïdes : application aux maladies à prion". Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066263/document.
Texto completoThe amyloid neurodegenerative diseases are characterized by the degeneration and the aggregation of specific proteins. These aggregation processes remain misunderstood by specialists and, mostly, only hypothetical. In this thesis, and in collaboration with biophysicists, we analyze the mechanisms of aggregation, relying on experimental data. Modeling is then a must. We present two models which we compare with the experiments. The first model, well-known from the literature is the Becker-Döring system. An infinite system of ordinary differential equations. This first model allows us to reproduce satisfactorily the early stages of the experiments. The second model we introduce is based on an additional hypothesis which is about the formation of different fibers. This second model allows us to reproduce the experiments
Sivera, Raphaël. "Modélisation et mesure de l'évolution morphologique du cerveau à partir d'IRM structurelles pour l'étude des maladies neurodégénératives". Thesis, Université Côte d'Azur (ComUE), 2019. http://www.theses.fr/2019AZUR4082.
Texto completoIn medical imaging, the statistical analysis of deformations enables the characterization of the effects of neurodegenerative diseases on the brain morphology. Deformations are able to capture precise changes but their analysis raises specific methodological challenges and the results may be difficult to interpret. The objective of this thesis is to present deformation-based methods and to show applications that contribute towards a better clinical interpretation of morphological changes. In the first part, we introduce a joint model of the effects of normal aging and Alzheimer’s disease on the brain morphology. The model proposes a simple description of both processes and is used to generate realistic and personalized evolutions under several diagnosis conditions. In the second part, a morphometric study is conducted on the MAPT cohort. We bring out an effect of the multidomain intervention on the longitudinal deformation of the brain using multivariate statistics. This effect is not observable using clinical assessments or volumetric measures, but we show that the differences associated with the treatment are correlated with better cognitive performance. The third part extends the statistical methodology used in the second part. A complete hypothesis testing framework for multivariate images is presented. It generalizes existing non-parametric frameworks and requires few hypothesis on the data to be applied. Finally the last part builds on the methodology of the previous sections to explore the relation between morphology and cognition in elderly subjects. The spatial correlations and the patterns of evolution described in this section suggest the existence of several dynamics of evolutions that are associated with specific cognitive changes
Sauty, Benoît. "Multimodal modelling of Alzheimer's Disease progression". Electronic Thesis or Diss., Sorbonne université, 2023. http://www.theses.fr/2023SORUS348.
Texto completoAlzheimer's disease (AD) is a multi-facet pathology, that can be monitored through a variety of data types. This thesis aims to leverage multimodal longitudinal data, especially imaging scans and cognitive tests, to provide a statistical description of the progression of AD and to enable individual forecasting of future decline. Mixed-effect disease progression models (DPMs) are commonly used for these tasks. In this context, our first contribution questions the frequent assumption that biomarkers follow linear or logistic functions over time, and we propose a geometric framework that assumes the data lie on a manifold and follow geodesics over time. We learn the Riemannian metric of the observation space and are able to model a wider variety of biomarkers, without priors on the shape of the trajectory over time. Using variational auto-encoders, we then extend this framework to neuroimaging data (MRI or PET scans), in order to provide high-dimensional progression models that describe the patterns of structural and functional alterations of the brain over the course of AD. We then apply this family of DPMs to clinical studies data in order to investigate the heterogeneity of AD progression, due to APOE-e4 genotype and sex on patterns of brain alterations. Lastly, we use said DPMs with a set of imaging and fluid biomarkers to identify the specific combinations of input features that best forecast cognitive declines in patients at different stages of the disease. The thesis demonstrates that DPMs can effectively model the progression of AD using a great variety of multimodal longitudinal data and provide valuable insights into the disease's clinical manifestations and progression. These findings can inform clinical trial design and facilitate more accurate prognosis and individualized treatment strategies for patients with AD
Gay, Marion. "Conception, synthèse et évaluation de composes interagissant avec la dégradation des protéines pour le traitement de maladies neurodégénératives". Thesis, Lille 2, 2015. http://www.theses.fr/2015LIL2S056.
Texto completoTwo physiopathological processes are involved in Alzheimer’s disease: the senile plaques (amyloid pathology) consisting of Aβ peptide aggregates and neurofibrillary tangles (Tau pathology) caused by the accumulation of hyper and abnormal phosphorylated Tau protein. Currently, only symptomatic treatments are available. Therefore, the development of curative drugs is a very active research field. Previous work in the laboratory led to the discovery of a family of compounds (MSBD) which lead-compounds are active on both pathologies of the Alzheimer’s disease. A drug candidate, AZP2006, emerged from that research and is currently in phase 1 clinical trials. Investigations on the identification of the biological target of AZP2006 led to p97/VCP protein, a target that has attracted considerable attention over the last few years for the treatment of neurodegenerative diseases (NDD).This PhD thesis deals with three main aspects:1) Study of the interactions between p97/VCP and developed compounds. STD-NMR studies have confirmed the interaction between AZP2006 and p97/VCP, though these preliminary results have to be confirmed by complementary techniques. AZP2006-based chemical probes were designed and synthesized to develop a FRET-based binding assay in order to get a more quantitative characterization of the binding.2) Development of new p97/VCP ligands. Based on previous ligands developed in the laboratory, a pharmacophore model was built. Subsequent, virtual screening and de novo design led to the identification of several chemical structures. Four families were synthesized and tested in vitro showing a good effect on Aβ peptides secretion and APP metabolism. These compounds are being tested on Tau hyperphosphorylation. The binding to p97/VCP was confirmed by STD-NMR.3) Development of multi target compounds acting on both the two pathology of Alzheimer disease and acetylcholinesterase (AChE). Activities of these compounds were validated in vitro (inhibition of AChE, Aβ peptides secretion, APP metabolism and Tau). In vivo, one of the compounds increased cognitive performance in two mice transgenic models.The results obtained during this PhD confirmed the therapeutic potential of p97/VCP in NDD and proposed new structures for their treatment
Berthommier, Frédéric. "Intégration neuronale dans le système auditif : modélisation de réseaux neuronaux temporo-dépendants". Phd thesis, Université Joseph Fourier (Grenoble), 1992. http://tel.archives-ouvertes.fr/tel-00342101.
Texto completoBerthommier, Frédéric. "Intégration neuronale dans le système auditif : modélisation de réseaux neuronaux temporo-dépendants". Phd thesis, Grenoble 1, 1992. https://theses.hal.science/tel-00342101.
Texto completoLenuzza, Natacha. "Modélisation de la réplications des Prions : Implication de la dépendance en taille des agrégats de PrP et de l'hétérogénéité des populations cellulaires". Phd thesis, Ecole Centrale Paris, 2009. http://tel.archives-ouvertes.fr/tel-00453321.
Texto completoSanches, Maria Clara Pires. "Language impairments in neurodegenerative diseases : function, dysfunction and modulation with transcranial stimulation". Thesis, Sorbonne université, 2019. http://www.theses.fr/2019SORUS669.
Texto completoLanguage is one of the most defining features of human beings and for centuries researchers have been interested on the functional organization of language and which neural substrates subtend its normal functioning. A breakdown of mechanisms subtending normal language abilities characterizes different neurodegenerative conditions, which have become models to study the neural basis and mechanisms of language processing. In the absence of effective treatments for language deficits in different neurodegenerative diseases, non-invasive brain stimulation approaches have been gaining momentum. Transcranial Direct Current Stimulation (tDCS) modulates neural activity via the induction of weak electrical intracranial currents, showing benefits in post-stroke and neurodegenerative aphasic patients. In this context, the studies included in this thesis analyzed neurodegenerative lesion models to characterize the behavioral mechanisms of word access and processing, address their impact on language abilities and explore the modulation of language impairment by means of tDCS to define its therapeutic value. The manuscript is divided in 4 chapters organized along three main axes: (1) fundamental research on language (2) clinical research on language breakdown and therapies and (3) impact of individual factors on the variability of the response to such therapies, an Introduction chapter and a General Discussion chapter
Libros sobre el tema "Modélisation des maladies neurodégénératives"
S, Harper Peter y Perutz Max F, eds. Glutamine repeats and neurodegenerative diseases: Molecular aspects. Oxford: Oxford University Press, 2001.
Buscar texto completoAbel, Lajtha y Vécsei Lázló, eds. Frontiers in clinical neuroscience: Neurodegeneration and neuroprotection : a symposium in Abel Lajtha's honour. New York: Kluwer Academic/Plenum Publishers, 2004.
Buscar texto completoAbel, Lajtha y Vécsei Lázló, eds. Frontiers in clinical neuroscience: Neurodegeneration and neuroprotection : a symposium in Abel Lajtha's honour. New York: Kluwer Academic/Plenum Publishers, 2004.
Buscar texto completoLes Maladies Neurodégénératives et Maladies Apparentées en Pratique. Elsevier, 2022. http://dx.doi.org/10.1016/c2018-0-00413-2.
Texto completoJeune, Rémy Le. Prévenir des maladies neurodégénératives grâce aux huiles essentielles. QUINTESSENCE, 2020.
Buscar texto completoPathogenesis of Neurodegenerative Disorders (Contemporary Neuroscience). Humana Press, 2001.
Buscar texto completoFrontiers in clinical neuroscience: Neurodegeneration and neuroprotection : a symposium in Abel Lajtha's honour. New York: Kluwer Academic/Plenum Publishers, 2004.
Buscar texto completoFrontiers in clinical neuroscience: Neurodegeneration and neuroprotection : a symposium in Abel Lajtha's honour. New York: Kluwer Academic/Plenum Publishers, 2004.
Buscar texto completo(Editor), Peter S. Harper y Max Perutz (Editor), eds. Glutamine Repeats and Neurodegenerative Diseases: Molecular Aspects. Oxford University Press, USA, 2001.
Buscar texto completoCapítulos de libros sobre el tema "Modélisation des maladies neurodégénératives"
Krolak-Salmon, P. y M. A. Hénaff. "Cognition sociale dans les maladies neurodégénératives". En Traité sur la maladie d’Alzheimer, 213–23. Paris: Springer Paris, 2013. http://dx.doi.org/10.1007/978-2-8178-0443-9_12.
Texto completoVlaicu, Mihaela Bustuchina˘ y Andrei Vlaicu. "Maladies neurodégénératives". En Neuromodulation en Neurologie et en Psychiatrie, 253–71. Elsevier, 2023. http://dx.doi.org/10.1016/b978-2-294-77862-9.00011-6.
Texto completoArnulf, I. "Maladies neurodégénératives et sommeil". En Les troubles du sommeil, 285–96. Elsevier, 2012. http://dx.doi.org/10.1016/b978-2-294-71025-4.00023-3.
Texto completoPlanche, Vincent. "Outils d’imagerie dans les maladies neurodégénératives". En Les Maladies Neurodégénératives et Maladies Apparentées en Pratique, 73–85. Elsevier, 2022. http://dx.doi.org/10.1016/b978-2-294-76331-1.00007-0.
Texto completoClary, Amandine, Gwenaëlle Galimard-Cloerec, Florence Keusch, Danièle Lafaye, Sophie Lefebvre, Bernard Paternostre y Laurent Pavageau. "Médecine palliative et accompagnement dans les maladies neurodégénératives". En Les Maladies Neurodégénératives et Maladies Apparentées en Pratique, 87–114. Elsevier, 2022. http://dx.doi.org/10.1016/b978-2-294-76331-1.00008-2.
Texto completoBobeuf, Florian, Nicolas Berryman y Louis Bherer. "Maladies neurodégénératives et activités physiques adaptées". En Guide d'intervention en activités physiques adaptées à l'intention des kinésiologues, 179–96. Presses de l'Université du Québec, 2020. http://dx.doi.org/10.2307/j.ctv1n35dcr.19.
Texto completoHoueto, Jean-Luc. "Histoire naturelle de la maladie de Parkinson idiopathique". En Les Maladies Neurodégénératives et Maladies Apparentées en Pratique, 239–51. Elsevier, 2022. http://dx.doi.org/10.1016/b978-2-294-76331-1.00019-7.
Texto completoDamon-Perrière, Nathalie. "Éducation thérapeutique". En Les Maladies Neurodégénératives et Maladies Apparentées en Pratique, 125–29. Elsevier, 2022. http://dx.doi.org/10.1016/b978-2-294-76331-1.00010-0.
Texto completoBrochet, Bruno. "Traitement médicamenteux de la sclérose en plaques". En Les Maladies Neurodégénératives et Maladies Apparentées en Pratique, 361–71. Elsevier, 2022. http://dx.doi.org/10.1016/b978-2-294-76331-1.00029-x.
Texto completoMontcuquet, Alexis y Laurent Magy. "Maladies apparentées à la sclérose en plaques". En Les Maladies Neurodégénératives et Maladies Apparentées en Pratique, 355–59. Elsevier, 2022. http://dx.doi.org/10.1016/b978-2-294-76331-1.00028-8.
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