Auswahl der wissenschaftlichen Literatur zum Thema „Organoïdes Cérébraux de Souris“
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Zeitschriftenartikel zum Thema "Organoïdes Cérébraux de Souris"
Guillon, Noëlle. „Des « organoïdes » cérébraux améliorés“. Pour la Science N° 558 – Avril, Nr. 4 (28.03.2024): 10–11. http://dx.doi.org/10.3917/pls.558.0010.
Der volle Inhalt der QuelleGaillard, Maxence. „Organoïdes cérébraux : de la conscience dans des systèmes microphysiologiques in vitro ?“ Revue de métaphysique et de morale N° 121, Nr. 1 (31.01.2024): 29–45. http://dx.doi.org/10.3917/rmm.241.0029.
Der volle Inhalt der QuelleDumouchel, Paul. „Ce que l'on peut apprendre sur les chauves-souris à l'aide d'une télé couleur“. Dialogue 32, Nr. 3 (1993): 493–505. http://dx.doi.org/10.1017/s0012217300012282.
Der volle Inhalt der QuellePAIN, Bertrand, Noémie AURINE, Théo LA ROSA, Camille BAQUERRE und Muriel COULPIER. „Potentiel des organoïdes cérébraux comme modèles d’étude des neuropathologies chez les animaux domestiques“. INRAE Productions Animales 36, Nr. 2 (13.09.2023). http://dx.doi.org/10.20870/productions-animales.2023.36.2.7637.
Der volle Inhalt der QuelleFermigier, Alice, Marc Dhenain und Clément M. Garin. „Étude comparative des réseaux cérébraux en IRM fonctionnelle au repos chez l’humain, le microcèbe et la souris“. Bulletin de l'Académie Vétérinaire de France 177 (2024). http://dx.doi.org/10.3406/bavf.2024.71070.
Der volle Inhalt der QuelleDissertationen zum Thema "Organoïdes Cérébraux de Souris"
Koshy, Aysis. „Characterization of Neural Development : Linking Retinoic Acid Receptors to Cell Fate and Modelling Tumorigenesis in Brain Organoids“. Electronic Thesis or Diss., université Paris-Saclay, 2023. http://www.theses.fr/2023UPASL119.
Der volle Inhalt der QuelleThe development of the Central Nervous system in the embryo depends on timely and precise signaling of molecules. Retinoic acid is one such molecule well characterized for its impact in brain and eye development. In its metabolically active form, ATRA (All Trans Retinoic acid) binds Retinoic acid receptors (RAR), and controls downstream gene expression attributed to cell maturation and apoptosis. The RAR exists as three isotypes - RARα, RARβ, & RARγ. During embryological development, each isotype is present in spatially distinct locations influencing patterning and maturation. The current state of research is limited to the correlation of a specific RAR isotype to a particular cell fate. In this thesis, we discuss findings that point to the ability of RARβ & RARγ to synergistically restore cell specialization by hijacking RARα-controlled gene programs. In a single-cell RNAseq approach, we are able to visualize several clusters unique to RARβ + RARγ activation during mouse stem cell differentiation beyond neuronal precursor stages. In a similar vein, studying nervous tissue development in the context of diseases is relevant to understanding disease characteristics and identifying targeted therapy options. With this in mind, we wanted to develop a mouse brain organoid (BORG) model from H3.3K27M and H3.3G34R mutant mouse ES cells as an invitro research model that is cost effective and reproducible. Here, we show proof of a tumorigenic like mouse BORG that harbors a TP53 knockout signature
Lozan, Ecaterina. „Analyse quantitative de l'Estradiol dans les tissus cérébraux et le plasma de souris“. Thesis, Bordeaux, 2015. http://www.theses.fr/2015BORD0390/document.
Der volle Inhalt der QuelleEstrogens are neurosteroids, especially Estradiol (17β-E2) which is considered to be the most biologicallyactive form. 17β-E2 could have positive effects on some age-associated anomalies (memory and cognitive impairment,Alzheimer's disease). For elucidating and better understanding the molecular and cellular mechanisms that underliethe effects within the brain, it is necessary to quantitate 17β-E2 and its metabolites (estrone and estriol) in brain andplasma.First, the RP-HPLC-ESI(-)-MS/MS method without derivatization was developed. The selectivity of the separationand the sensitivity of detection of the estrogens has been improved after optimization of MRM and chromatographicparameters.Secondly, the various derivatization agents were evaluated after their synthesis in order to improve the sensitivity,selectivity and signal enhancement. After studying the eleven synthesized derivatives of 17β-E2 in ESI-MS andMS/MS, promising results were obtained with the 17β-E2-Q8S derivative.A simple purification method using liquid-liquid extraction followed by C18 solid phase extraction has been optimizedin order to minimize assay interferences. The two assays (with and without derivatization) were then compared interms of efficiency, detection and quantification limits (LOD/LOQ), calibration linearity and reproducibility. Then,both methods were validated on biological samples (brain, hippocampus and plasma) collected from animals treatedwith known amounts of 17β-E2. Finally, the more robust method was the method without derivatization with a LODof 0.5 fmol.μL-1
Degiorgis, Laetitia. „Analyse des réseaux cérébraux par IRM chez un modèle souris de la maladie d’Alzheimer“. Thesis, Strasbourg, 2019. http://www.theses.fr/2019STRAD025.
Der volle Inhalt der QuelleAlzheimer’s disease (AD) is the most widespread dementia in the world, presenting progressive memory impairment. Using resting-state MRI, in both human and animal studies, has opened a new window into the brain and its connectome, proposing abnormal functional connectivity as a candidate biomarker of brain pathologies such as AD. We investigated the connectome’s affectation over time in vivo in a longitudinal study, to follow-up and characterize a transgenic mouse model of AD, combining both functional and structural approaches and evaluating possible network signatures of pathological states. We associate behavioral assessment and histological staining of neurotoxic protein to the MRI approach, in order to relate pathological mechanism, at both network and cellular level, to memory dysfunction. We found remarkable structural and functional modifications, mediating prodromal alterations of the memory system, before the beginning of memory impairment. Considerable changes in the septal connectivity particularly towards limbic centers but also involving communication with the Default Mode Network were highlighted over time. These vulnerable circuits represent biomarkers of the disease and potential targets for future treatment
Porte, Baptiste. „Étude structurale des microvaisseaux cérébraux chez la souris au cours du développement périnatal par des approches protéomique et transcriptomique“. Rouen, 2015. http://www.theses.fr/2015ROUENR04.
Der volle Inhalt der QuelleNeonatal acquired brain lesions have various origins and result in lasting disabilities requiring long term expensive care. Usually identified as cerebral palsy (CP), these disabilities have not decreased in the last two decades, even if neonatal cares underwent improvements. The nature of brain lesions resulting in CP are highly dependent on when the developing brain is exposed to insults and less on insulting event, indicating the determinant part of brain parenchyma and vasculature maturity dependent context. Brain vascular endothelial cells (BEVC) represent an exchange interface between blood and brain. In fact, they support blood brain barrier (BBB) functions: i) physical barrier, ii) transendothelial transport, and iii) metabolic barrier. These functions are assumed by specific protein sets expression in BEVC: i) tight junction (claudins, junction adhesion molecules, occludin) and adherent junction proteins (cadherins, catenins), ii) transporters (solute carriers), and iii) metabolic barrier proteins (enzymes, ATP-binding cassette proteins, multi-drug resistance proteins). BBB functions appear progressively along with development, although permeability is reduced early in fetal life. The roles for vascular reactions in the etiology of lesions likely depend on this "maturity", as highlighted by the high prevalence of intraparenchymal hemorrhages affecting selectively extreme preterms. Previous studies in the laboratory identified differences between neonate and adult BVEC in culture, both at structural and functional levels (energy transport proteins, proteases secretion and glutamate sensitivity). These properties, likely involved in tissue development, may also be responsible for its peculiar vulnerability to environment factors. Other studies in the laboratory showed that five day-old (P5) mice pups were prone to develop hemorrhage while eight day-old pups were resistant in a t-PA inhibitor (PAI-1) knock-out transgenic strain. The aim of this thesis was to characterize factors putatively involved in microvessels vulnerability. In this attempt, we have studied the proteome and the transcriptome dynamic in forebrain microvessels (fMV) from P5 and P10 pups, and adult mice. Indeed, data from the literature allow considering P5 and P10 mice as preterm and full term human neonates surrogates, in terms of cortical maturity. The study has been performed using two independent proteomic and transcriptomic approaches applied to a common biological material: purified fMV from P5, P10 and adult mice. Proteome study was performed using a nanoLC LTC-Orbitrap (Thermo Fischer Scientific) mass spectrometer allowing protein contents analysis (MS/MS) after tryptic digestion. The MS/MS study allowed identification and quantification of 632, 727 and 692 proteins in P5, P10 and adult mice fMV, using Proteome Discoverer® and Progenesis IC-MS® softwares with Mascot® identification based on IPI databank. Fifty-two percent of the 899 unique proteins identified were common to the three ages. The quantitative analysis revealed the highest protein diversity and levels at P10. Protein lists classification by Gene Ontology using KEGG pathways (DAVID online freeware) allowed the identification of pathways significantly over-represented. Although pathways were common at the 3 stages, they exhibit different contents in particular on i) intercellular gap and tight junctions, ii) focal adhesion molecules to basal lamina, iii) basal lamina components and iv) transporters. Gene transcripts dynamic regulations were studied by cRNA hydrization against probes covering whole mouse genome, spotted in Agilent® arrays. Three parallel analyses, each based on cRNA competitive hydrization of from two samples labeled with different fluorochromes, allowed to evaluate expression dynamics (P5-P10, P10-Adult P5-Adult) using the GeneSpring® software. In total, 3197 and 2821 genes exhibited a two-fold minimum up-or down-regulation in at least one comparison. The Gene Ontology study allowed extraction of 92 pathways with significant over-representation in the whole study. Most of those pathways were related to metabolism and signal transmission. Comparisons involving P10 samples exhibited pathways related to cell adhesion. Directed surveys towards BBB (junctions, transport and efflux functions), proteases and glutamate transmission were done manually since mice ontology databanks did not recorded these pathways. Ontology data from proteome and transcriptome studies pointed out a common observation that within pathways detected at all the stages in our study, the unitary elements involved (protein or gene) were largely replaced. This observation was done on basal lamina elements and cell adhesion factors, transport proteins, glutamate transmission, proteases and their inhibitors. Theses data support the hypothesis that the transient vulnerability of microvessels responsible for brain hemorrhages is due to a particular constitution of microenvironment together with a high proteolytic potential, occurring at P5 in mice
Boutonnet, Marie-Charlotte. „Caractérisation des oligomères β-amyloïdes cérébraux et vasculaires impliqués dans la maladie d’Alzheimer“. Thesis, Bordeaux 1, 2013. http://www.theses.fr/2013BOR14997/document.
Der volle Inhalt der QuelleAlzheimer's disease (AD) is a complex disorder of the central nervous system that affects an increasing number of people worldwide due to the overall aging of the human population. Vascular factors and mechanisms have emerged as an area of key importance. Accumulating evidence indicates that pre-fibrillar aggregates, specifically the low-molecular weight oligomers of Aβ peptide, are responsible for the synaptic dysfunction and neuronal loss that occur in AD pathology. But, these oligomeric forms implicated in the pathology are currently under debate. Our primary goal was to identify cerebral and vascular oligomeric signatures. Secondly, we try to interfere with these signatures in order to modify the evolution of AD. We realize qualitative analyses of cerebral and vascular oligomers Aβ by western-blot. Vascular and cerebral tissues were extracted from AD patients and from a transgenicmouse model of AD. We demonstrate that the same oligomer Aβ (17-18 kDa) is implicated in the cognitive impairment for patients and APP/PS1 mouse. A specific vascular signature of oligomer Aβ was detected in peripheral vessels and particularly in portal vein from liver of APP/PS1 mouse. Moreover, pharmacological treatment targeting clearance of soluble Aβ restored the control signature of oligomer Aβ in the brain of APP/PS1 mouse. This configurational change was associated with an increase of oligomer Aβ in portal vein from liver. These results show that cerebral and vascular oligomeric signatures were closely linked. Finally, our work emphasizes potential therapeutic strategies for AD by targeting cerebrals and vasculars oligomers Aβ
Nassor, Férid. „Etude de mécanismes de type prion impliqués dans la maladie d’Alzheimer sur un modèle de mini-cerveaux humains avec exploration par microscopie 3D“. Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS105.
Der volle Inhalt der QuelleHuman neurodegenerative diseases, which are all based on prion-like mechanisms (self-propagation of pathogenic protein aggregates), represent a major societal risk with the increase of their prevalence directly correlated to the increasing longevity of the world population. There is to date neither any cure nor any pertinent experimental model for their study.The objective of this work was to use the potential of human mini-brains, a self-assembled three-dimensional in vitro model able to restitute the complexity of the cerebral cortex. This model will allow us to study prion-like mechanism by developing a validation methodology based on 3D microscopy. These novel 3D structures can be obtained from reprogrammed adult cells into induced pluripotent stem cells (iPSCs) and offer unique possibilities to access, observe and disrupt biological processes in the human brain without bias nor complications as in animal models and ex vivo human brain samples. This model makes it possible to observe the development of aggregates of Aβ and hyper-phosphorylated Tau, two proteins that accumulate and propagate from cell to cell during Alzheimer’s disease.We have been to able to adapt the cerebral organoid model for a future screening approach by modifying the differentiation methodology to enhance its production ratio. We also have been able to test different modalities for disease modeling for Alzheimer’s disease, Parkinson’s disease, Fronto-Temporal Dementia and Creutzfeldt-Jakob disease: with chemical induction, with patient specific cells, through genetic modification and through contact with infectious material. These different approaches allowed us to validate that the cerebral organoid can indeed reproduce key aspects found during pathological development within patients. To compensate for the heterogeneity of the cerebral organoid, we performed an in toto analysis through microscopy, meaning in its totality without prior slicing. The chosen method of acquisition is fluorescence light-sheet microscopy used after staining and optical clearing of cerebral organoids. To do so, we have evaluated and established different strategies in order to obtain a high content screening platform for our cerebral organoid model.This platform centered around the cerebral organoid model, underpinned by 3D microscopy analysis, was developed during the “Investissements d’Avenir” project 3DNeuroSecure. This project has for ambition to bring high performance computing to the biological sciences, notably with the possibility to deal with large scale data, also called “exascale”, like the ones obtained with 3D microscopy. The development of this aspect would allow us to establish the basis for a therapeutic screening tool based on cerebral organoids for neurodegenerative diseases. We have demonstrated that prion-like mechanisms can be studied in a human mini-brain model and multiple research avenues are now opened for both fundamental and applied research. This platform could in turn become the basis for any kind of organoids derived from patients to model the whole human body and become a biological companion for personalized medicine
Ricard, Clément. „Effets de la photoactivation par irradiation synchroton sur la microvascularisation et sur les tissus cérébraux chez la souris saine ou porteuse d'un gliome : développements en microscopie biphotonique et essais précliniques“. Grenoble 1, 2008. http://www.theses.fr/2008GRE10081.
Der volle Inhalt der QuelleBrain tumors are the third most frequent pathology encountered in neurology following stroke and dementia. Approximately 10 new cases are encountered each year in a population of 100. 000. Glioblastoma are the most aggressive among brain tumors and despite medical progress they suffer of a poor prognosis (median survival time is 12 months; five years survival rate is 2%). One of the challenges in neuro-oncology is the development of new curative treatments against glioblastoma. One of them, the photoactivation therapy of platinum with synchrotron X-rays (PAT-Plat) was developed during the last years and has shown curative effects in rats bearing the F98 glioma. In the present study, we have attempted to characterize the effects of the PAT-Plat and its different modalities (chemotherapy with cisplatin and synchrotron radiotherapy) on healthy brain tissue and microvasculature as well as on the F98 glioma. Intravital multiphoton microscopy was used as the main imaging tool to investigate the effects of the PAT-Plat and many methodologies were developed (assessement of blood-brain-barrier (BBB) disruption, imaging of tumor microvasculature, staining of astrocytes and elastic fibers). We have shown that a 15Gy/79keV synchrotron irradiation does not induce short term side effects (BBB disruption, diminution of the perfusion, gliosis,. . . ) in the parietal cortex of nude mice. We have also demonstrated that a synergystic effect between cisplatin and irradiation is at the origin of the effects of the PAT-Plat. Finally, we have shown that the action of the PAT-Plat is not restricted to tumor cells; a decrease in the angiogenic vessels perfusion was also observed in the peritumoral area of the F98 glioma
Bucur, Adriana. „Spectométrie de RMN quantitative in vivo pour la mesure des lipides hépatiques chez l'homme et des métabolites cérébraux chez un modèle murin de neuro-inflammation“. Thesis, Lyon 1, 2010. http://www.theses.fr/2010LYO10094.
Der volle Inhalt der QuelleThe proton MRS is a unique non-invasive method to quantitative biochemical exploration of living tissues. The studies presented in this thesis aim to handle each one of the involved steps, from data acquisition to reliable and precise metabolic profile estimation of explored tissues. Protocols for experimental acquisition of in vivo, short echo-time magnetic resonance signals were defined, and optimized for a pre-clinical application (mice) on a 4.7T scanner and for a clinical study at 1.5T. The first study allowed yo measuring cerebral metabolite (N-acetyl-aspartate, choline, creatine, taurine) alterations along time in a murine model of neuro-inflammation on a 4.7T scanner and the second study aimed to measure the total quantity and the composition of liver fat in patients with hepatic steatosis in a clinical environment at 1.5T. Signal processing methods for metabolite and fat contribution estimates, coping with physical signal properties were validated for both studies. These methods are based on non-linear least squares algorithms. Multiple starting values and constraints strategies were successfully validated. The assets and the originality of this project are based on the synergic developments of acquisition protocols and the associated signal processing methods. These developments were designed to enrich the list of the biochemical information non-invasively measured, in order to help medical prognostic and diagnostic
Daher, Ismail. „Etude neurochimique et comportementale des effets neuroprotecteurs du MgSO4 à court et long termes dans deux modèles de lésion cérébrale périnatale chez la souris mâle et femelle“. Rouen, 2016. http://www.theses.fr/2016ROUES039.
Der volle Inhalt der QuellePrematurity is responsible for neonatal mortality and morbidity. Premature infants are at risk of developing cerebral palsy (CP), characterized by motor and cognitive deficits lasting until adulthood. Hypoxia-ischemia, inflammation and male gender have been identified as CP risk factors. Magnesium sulfate (MgSO4) have been proposed as neuroprotective agent to improve infants sensorimotor and cognitive outcomes. Despite the reduction of CP prevalence by 33 %, MgSO4 use in clinic remains not systematic, notably in France, since its long term proper effects and its actions mechanisms are not well-known. Our work consisted in improving the knowledge of MgSO4 actions and effects. In order to evaluate MgSO4 (600 mg/kg) preventive actions mechanisms and its potential proper effects, two mouse models of cerebral neonatal lesion at 5 days (P5) have been used. We showed that the excitotoxic model (IBO), as the hypoxic-ischemic model (HI), have induced sensorimotor deficits in pups in both sexes, as motor and cognitive deficits in adult mice, more pronounced in male mice in the IBO model. In the latter, MgSO4 administration prevented at short and long term sensorimotor and cognitive alterations, as well as glutamatergic and GABAergic neurotransmissions systems alterations. In the HI model, which causes more severe lesions, cognitive deficits have not been prevented by MgSO4. We also showed that MgSO4 induced neuroprotection is multifactorial, as MgSO4 reduced glutamatergic neurotransmission and apoptosis. Work in progress in the HI model indicates that MgSO4 may decrease inflammatory process, in a sex dependant manner. MgSO4 pre-treatment did not induce deleterious secondary effects in the measured parameters in our study
Fillinger, Clémentine. „Identification du connectome de l'aire 24 du cortex cingulaire antérieur dans le contexte du développement de phénotypes de type anxio-dépressif chez la souris : implication de la voie amygdalo-cingulaire“. Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ029/document.
Der volle Inhalt der QuelleThe anterior cingulate cortex (ACC) is a prefrontal region located at the center of a network allowing the sharing of cognitive, motor, limbic and visceral information, placing it as an interesting target for the study of complex pathologies like mood disorders. To investigate these diseases in mice, we provided the complete connectome of each ACC areas by a tract-tracing approach. We demonstrated that the majority of structures constituting this connectome are reciprocally connected with the ACC and that some density and topographical connection specificities were observed among cingulate areas. These results potentially suggest some shared functions between cingulate areas, also completed by specific roles inherent to each area. Using this connectome, we demonstrated that the repeated activation of the amygdala projection to the ACC was able to induce anxiodepressive-like behaviors in naïve mice, by using optogenetics combined with behavioral tests. This study highlights for the first time the implication of a portion of the ACC connectome in the establishment of mood disorders