Auswahl der wissenschaftlichen Literatur zum Thema „Troubles du neurodéveloppement“
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Zeitschriftenartikel zum Thema "Troubles du neurodéveloppement"
Gressens, Pierre. „Troubles du neurodéveloppement?: mécanismes“. Contraste N°51, Nr. 1 (2020): 11. http://dx.doi.org/10.3917/cont.051.0011.
Der volle Inhalt der QuelleDes Portes, Vincent. „Troubles du neurodéveloppement?: aspects cliniques“. Contraste N°51, Nr. 1 (2020): 21. http://dx.doi.org/10.3917/cont.051.0021.
Der volle Inhalt der QuellePurper Ouakil, D. „AFPBN – Bases des actions précoces et préventives dans les troubles du neurodéveloppement“. European Psychiatry 30, S2 (November 2015): S70. http://dx.doi.org/10.1016/j.eurpsy.2015.09.330.
Der volle Inhalt der QuellePry, René. „Wallon, le neurodéveloppement et ses troubles“. Enfance N° 3, Nr. 3 (02.09.2022): 337–51. http://dx.doi.org/10.3917/enf2.223.0337.
Der volle Inhalt der QuelleLeroy Malherbe, Véronique, und Gwenaëlle Lefévère-Renard. „Les troubles moteurs des enfants porteurs de troubles du neurodéveloppement“. Contraste N°51, Nr. 1 (2020): 161. http://dx.doi.org/10.3917/cont.051.0161.
Der volle Inhalt der QuellePlumet, Marie-Hélène. „Troubles de la communication sociale et neurodéveloppement“. Contraste N°51, Nr. 1 (2020): 241. http://dx.doi.org/10.3917/cont.051.0241.
Der volle Inhalt der QuelleCHASTANG, J., E. BOUSSARSAR, B. CHAVANNES, K. BONELLO, A. DE OLIVEIRA, JS CADWALLADER und G. IBANEZ. „QUELS SONT LES FACTEURS ASSOCIES A LA QUALITE DE VIE DES PARENTS D ENFANTS ATTEINTS DE TROUBLES DU NEURODEVELOPPEMENT EN ILE-DE-FRANCE ?“ EXERCER 34, Nr. 194 (01.06.2023): 244–51. http://dx.doi.org/10.56746/exercer.2023.194.244.
Der volle Inhalt der QuellePurper-Ouakil, Diane. „Le trouble déficit d’attention hyperactivité (TDAH) dans les troubles du neurodéveloppement (TND)“. Contraste N°51, Nr. 1 (2020): 189. http://dx.doi.org/10.3917/cont.051.0189.
Der volle Inhalt der QuelleGeorgieff, Nicolas. „Intersubjectivité et troubles du neurodéveloppement?: l’autisme est-il un trouble des «?cognitions sociales?»??“ Contraste N°51, Nr. 1 (2020): 229. http://dx.doi.org/10.3917/cont.051.0229.
Der volle Inhalt der QuelleVallée, Louis, und Pierre Delion. „La consultation conjointe dans les troubles du neurodéveloppement : consulter ensemble“. L'information psychiatrique 98, Nr. 4 (01.04.2022): 281–85. http://dx.doi.org/10.1684/ipe.2022.2409.
Der volle Inhalt der QuelleDissertationen zum Thema "Troubles du neurodéveloppement"
Salvador-Prince, Lucie. „Impact des pesticides sur le neurodéveloppement et la maladie d'Alzheimer“. Thesis, Université de Montpellier (2022-….), 2022. http://www.theses.fr/2022UMONT009.
Der volle Inhalt der QuelleThe massive use of pesticides in the world causes pollution of all environments and contamination of foodstuffs by multiple residues. Many epidemiological studies show some correlations between high exposure to pesticides and neurodevelopmental pathologies such as autism or ADHD (attention deficit disorder with or without hyperactivity). Neurodevelopment corresponds to a period of susceptibility to environmental pollutants and according to Thomas Arendt's hypothesis, alterations during neurodevelopment, and in particular the corticogenesis, could have repercussions on brain aging by promoting the development of neurodegenerative diseases. However, it is difficult from an epidemiological point of view to determine the impact of in utero exposure to low doses of pesticides and throughout life on the human brain. It is therefore important to mimic this silent contamination on animal models. After having shown that chronic exposure to low doses of fungicides (cyprodinil, mepanipyrim, pyrimethanil) induced an aggravation of Alzheimer's disease (AD) markers in the J20 transgenic mouse model (Lafon PA. et al., 2020), we asked whether in utero exposure to these same compounds could: (i) induce neurodevelopmental defects; and (ii) whether these neurodevelopmental defects could lead to dysregulation of AD markers during aging.Based on this hypothesis, we set up a model of mother to child contamination, in which wild-type females were exposed during gestation, either to fungicide alone, or to a cocktail of the three fungicides (cyprodinil, mepanipyrim and pyrimethanil) to the dose of 0.1 μg/L/pesticide (regulatory dose authorized in distributed water in Europe). A first study of the brains of newborns, at 3 days postnatal (P3), showed that gestational exposure to fungicides has an impact on neurogenesis with an increase in Nestin+ neural precursors and DCX+ immature neurons, and a decrease in NeuN+ mature neurons, linked to the PI3K/Akt and Wnt/β-catenin signaling pathway. An extraction of adult neural stem cells from mice treated for 4 months revealed an increase in their proliferation and differentiation properties, but paradoxically a reduction in their migration property. In addition, changes in the expression of post-synaptic proteins, such as PSD95 and NMDA receptors, have been identified (Wang et al., 2021). To go further, we analyzed the hippocampal synaptic activity of the mice exposed in utero to the cocktail of fungicides at P10, P18 and P30. The results showed that in mice treated with the cocktail of fungicides, some changes occured in the ratio of NMDA/AMPA glutamate receptors, a defect in synapse maturation with a delay in the GluN2a/GluN2b subunits switch during development, epileptic or poly-synaptic type signals and a synaptic plasticity defect (LTD). We also studied corticogenesis in newborns at P10 exposed in utero to the cocktail of fungicides, thanks to an in utero electroporation technique with multi-color fluorescent tracers "MAGIC markers" which allow to follow the progeny of neural precursors. The results showed that the treated mice exhibit defects in the morphology and organization of neurons, as well as in the formation of cortical layers. To complete, behavioral studies have shown that mice exposed in utero to the cocktail of fungicides exhibit hypoactivity and memory defects. Finally, mice treated from gestation and up to 6 and 9 months of age are subjected to biochemical and histological analyzes in order to determine whether exposure to fungicides can have an impact on the increase of Alzheimer's disease markers during aging
Margarido, Pinheiro Vera. „L’interactome de Scrib1 et son importance pour la plasticitè synaptique & les troubles de neurodéveloppement“. Thesis, Bordeaux, 2014. http://www.theses.fr/2014BORD0318/document.
Der volle Inhalt der QuelleThe brain is made up of billions of nerve cells, or neurons. Neurons communicate with each other through functionally distinct structures - the axon and the dendrite - which are able to release and receive an electrical or chemical signal from a pre- to a post-synaptic compartment, respectively. We focused our study on hippocampal neurons synapses, which ultimately underlie high-order brain functions, such as learning and memory. In particular, we studied the development and maintenance of dendritic spines, whose changes in morphology are intimately correlated with synaptic plasticity, or the ability to respond to synaptic activity. Dendritic spines originate from motile dendritic filopodia, which mature into spines following axonal contact. The filopodia-to-spine transition involves a plethora of molecular actors, including glutamate receptors, scaffold proteins and the actin cytoskeleton, able to receive, transmit and integrate the pre-synaptic signal. The spatial and temporal coordination of all these molecular components throughout the formation and maturation of a synapse remains, however, unclear. Scribble1 (Scrib1) is planar cell polarity protein (PCP) classically implicated in the homeostasis of epithelial tissues and tumour growth. In the mammalian brain, Scrib1 is a critical scaffold protein in brain development and function. The main goal of this work was, therefore, to investigate the molecular mechanisms underlying Scrib1 role in synapse formation and maintenance. In a first part, we depict the importance of Scrib1 PDZ-dependent interactions on glutamate receptors trafficking as well as bidirectional plasticity signalling pathway underying spatial memory. In a second part, we focus on the functional consequences of a recently identified autism spectrum disorder (ASD) mutation of Scrib1 on neuronal morpholgy and function. We demonstrated that Scrib1 regulates dendritic arborization as well as spine formation and functional maintenance via an actin-dependent mechanism, whose disruption might underlie the ASD phenotype. Taken altogether, this thesis highlights the PCP protein Scrib1 as key scaffold protein in brain development and function, playing a plethora of roles from the subcelular to the cognitive level
Chastang, Julie. „Troubles du neurodéveloppement de l’enfant : vécu des parents et des enseignants, qualité de vie et outil de repérage“. Electronic Thesis or Diss., Sorbonne université, 2023. http://www.theses.fr/2023SORUS598.
Der volle Inhalt der QuelleIn France, neurodevelopmental disorders (NDD) affect 10 to 15% of children. Early detection of NDD is of crucial importance due to the maximum brain plasticity in the first 3 years of a child's life. Early detection should allow children to access early interventions that optimize their neurodevelopmental trajectory. This thesis initially focused on the experiences of parents of children with NDD and their quality of life. Parents described a complex journey, marked by waiting times for diagnosis which had significant repercussions on their quality of life, difficulties in accessing care, as well as a challenging journey facing the challenges related to their child(ren)'s schooling. Being supported by their primary care physician seemed to enhance their quality of life, while the delay to diagnosis negatively impacted it. Complementarily, this thesis also studied the experiences of teachers. It emerged that many of the difficulties identified by parents are shared by teachers. Both parents and teachers reported feelings of abandonment and loneliness in addressing the children's needs. They shared observations about the difficulties in identifying disorders, delays in diagnosis, complicated pathways, and a lack of support and resources. A recurring theme was the lack of coordination between parents, teachers, and the healthcare sector. Given the finding that no readily accessible tool existed for frontline use to identify deviations from the expected neurodevelopmental trajectory, a multidisciplinary group of experts was convened under the auspices of the inter-ministerial delegation to the national strategy for autism and neurodevelopmental disorders. This working group developed a detection grid based on existing literature and pre-existing tools, and this grid has been usable since 2019. The purpose of this thesis was to evaluate, for the first time, the use of this detection grid in the general population in primary care. The results obtained align with existing literature regarding the expected prevalence of NDD at the tested ages and factors associated with early identification of deviations in the neurodevelopmental trajectory. In summary, this thesis sought to explore the experiences of parents and teachers and the challenges they face, highlighting the complexities in the life journey of children with NDD and their families. From these observations, it aimed to find a solution for early detection of NDD by introducing, for the first time in primary care, a tool for detecting NDD
Gay, Olivier. „Marqueurs neurodéveloppementaux en psychiatrie : intérêt dans les troubles schizophréniques“. Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB016/document.
Der volle Inhalt der QuelleThe term neurodevelopment in its broadest sense refers to all of the processes encompassing development of the nervous system from the earliest stages of formation in utero to later stages of maturation during adolescence to produce the fully functional adult nervous system. Work over the last thirty years has led to a neurodevelopmental model of human psychiatric disorders, including schizophrenia, based on genetic, epidemiological and imaging evidence. This model asserts that disease is fundamentally linked to or develops from abnormality(s) in the formation processes (early neurodevelopment) and maturation (late neurodevelopment) of the nervous system due to a combination of genetic and environmental factors. In this context this thesis aims to clarify the effects of neurodevelopmental abnormalities on psychiatric disorders, including schizophrenia, through the study of different markers. The first study aims to investigate correlations between markers of early brain development: a clinical marker (neurological soft signs) and an imaging marker (sulcation of the cerebral cortex) in a population of subjects with schizophrenia. A correlation between these two markers is presented: the sulcation index was found to be lower in subjects that had significant neurological soft signs. We concluded that the combined study of different markers may help to isolate subgroups of patients with greater early neurodevelopmental damage. The second study aims to characterize effects of different markers of early neurodevelopmental abnormalities on cognitive functioning in patients with schizophrenia. Effects on executive control (as measured by the Trail Making Test) were correlated with clinical markers (neurological soft signs, handedness) and imaging (sulcation of the anterior cingulate cortex and enlargment of the ventricles). We found interactions between different markers with a mainly non-linear summation effect. Our interpretation is that different markers reflect separate insults, though all early, on brain development with a common final effect on executive function. The third study aims to clarify the specificity of sulcation as a marker of early neurodevelopmental abnormalities by studying a population of adult subjects with autism spectrum disorder (ASD), a patholody beginning in early childhood and linked with evidence of early neurodevelopmental damage. Sulcation abnormalities of the anterior cingulate cortex, similar to those observed in patients with schizophrenia are detected in patients with ASD. These results suggest early neurodevelopmental abnormalities are shared by different psychiatric disorders and that changes in cortical sulcation are not specific to a given disorder but the early damage. In conclusion, we suggest that the study of neurodevelopmental abnormalities should be integrated into a dimensional approach in psychiatry
Dupont, Charkaluk Marie-Laure. „Prématurité et neurodéveloppement : analyse longitudinale et recherche de facteurs pronostiques précoces à partir de l'étude de la cohorte EPIPAGE (Enquête épidémiologique sur les petits âges gestationnels)“. Paris 6, 2011. http://www.theses.fr/2011PA066485.
Der volle Inhalt der QuellePujol, Camille. „Le récepteur 5-HT6 et la dynamique de son réceptosome : rôle dans la différenciation neuronale et potentiel thérapeutique pour le traitement des troubles du spectre de l’autisme“. Thesis, Montpellier, 2018. http://www.theses.fr/2018MONTT059.
Der volle Inhalt der QuelleCognitive symptoms observed in neurodevelopmental pathologies such as schizophrenia or autism spectrum disorders are highly debilitating and poorly controlled by currently available treatments. Accordingly, there is still an urgent need for new therapeutic approaches. It has become clear in the last few years that these cognitive deficits are caused by neurodevelopmental alterations. The 5-HT6 receptor has emerged as one promising targets for the treatment of these deficits in light of its early expression during brain development, its role in key neurodevelopmental processes such as neuronal migration ad neurite growth and the pro-cognitive effects of antagonists in various cognitive tasks in rodents. In order to identify novel molecular substrates of the control of cognition and neural development by 5-HT6 receptors, our team has recently characterized the receptor interactome thanks to complementary proteomic strategies. Further functional studies revealed that the Cdk5 pathway under the control of 5-HT6 receptor plays a crucial role in in the migration and positioning of cortical pyramidal neurons as well as in the initiation of neurite outgrowth. The new protein partners of the receptor identified also include G protein-regulated inducer of neurite outgrowth 1 (GPRIN1), a Cdk5 substrate, known to promote neurite outgrowth. This thesis aims at characterizing the impact of the 5-HT6 receptor/GPRIN1 interaction upon receptor activity and neuronal differentiation in a neuroblastoma cell line (NG108-15 cells) commonly used as a cellular model for studying molecular mechanisms underlying neuronal differentiation. I showed that GPRIN1 interacts with a receptor sequence comprising the 22 N-terminal residues of its C-terminal domain via a mechanism depending on its association with activated Gαs protein and regulated by receptor phosphorylation at Ser350 by Cdk5, thus demonstrating that the receptor recruits either Cdk5 or GPRIN1 in a dynamic manner. I then showed that the physical interaction between GPRIN1 and the 5-HT6 receptor stabilizes an active receptor conformation able to activate Gs and the production of cAMP in an agonist-independent manner and exhibiting a low apparent affinity for inverse agonists. This interaction also promotes neurite extension and branching both in NG108-15 cells and primary cultured neurons originating from different regions of the mouse brain. These effects upon neuronal differentiation are mediated by agonist-independent activation of the Gs/adenylyl cyclase/PKA pathway. Collectively, my results indicate that neuronal differentiation under the control of 5-HT6 receptors requires a complex sequence of signaling mechanisms that depends on the sequential association of the receptor with Cdk5 and GPRIN1: while the 5-HT6/Cdk5 interaction is required for the initiation of neurite growth, neurite extension and branching depends on receptor association with GPRIN1. Finally, I demonstrated that sub-chronic administration to mice depleted of Mu opioid receptor (Oprm1-/- mice, preclinical model of autism spectrum disorders - ASDs -) improves a range of primary symptoms, including alteration of social cognition and stereotypic behaviors, suggesting that 5-HT6 receptor blockade might be a relevant strategy for the treatment of some behavioral symptoms in ASDs. Collectively, this thesis highlights the role of the 5-HT6 receptor interactome and of its dynamics in neuronal differentiation and the establishment of neuronal connectivity and opens new perspectives for the treatment of psychiatric disorders of neuro-developmental origin, such as ASDs
Zhang, Xinyan. „Uncovering the sleep pathway in the social profile of Rett syndrome“. Electronic Thesis or Diss., Lyon 1, 2022. http://www.theses.fr/2022LYO10128.
Der volle Inhalt der QuelleSleep is essential for maintaining optimal health. In children with neurodevelopmental and psychiatric disorders, problematic sleep is found with greater frequency and severity. Furthermore, problematic sleep is associated with poorer psychosocial functioning during the daytime. Rett Syndrome (RTT), one of the most common and severe genetic multi-disabilities in females, is strongly linked to the mutant methyl-CpG binding protein 2 gene (MECP2) on the X chromosome. Variant phenotypic forms of RTT present a spectrum of symptomatology similar to that of classical RTT but show subtle differences in some clinical features, including the Early Seizure Variant (ESV, Hanefeld variant, linked to mutant gene X-linked cyclin-dependent kinase-like 5, CDKL5), congenital variant (CV, Rolando variant, linked to the forkhead box G1 gene, FOXG1) and preserved speech variant (PSV, Zappella variant, also linked to MECP2). RTT affects 1 in 10,000 to 15,000 births, which represents 40 to 50 new cases each year in France. RTT is characterized by developmental arrest around 6-18 months after birth, the presence of stereotypical hand movements, and gait abnormalities coinciding with the loss of acquired purposeful hand skills and spoken language. The child withdraws socially. Other signs also described in RTT clinical profiles include epileptic seizure, breathing difficulties, abnormal muscle tone, scoliosis/kyphosis, as well as disturbed sleep. Accumulating pathophysiological findings in RTT suggest abnormal cortical activities and dysmaturity of the brainstem function, which is key in maintaining proper status during sleep or wakefulness. However, there is no scientific study investigating the relationship between sleep abnormalities and social impairments in RTT. Therefore, this doctoral work is subjected to this topic to link the day and night together in RTT. First, we undertook five systematic reviews of all previous studies on non-verbal social performance and sleep in RTT. Then, we analyzed polysomnographic recordings in a clinical sample of RTT individuals with MECP2 mutations. We studied their sleep macrostructure and respiration during sleep. In addition, we examined possible phenotypic traits via a stratified analytical approach to clinical and genetic characteristics. Lastly, to examine social profiles in RTT individuals, we extracted 25 social behavior items from the Rett Syndrome Behavior Questionnaire, and correlated them to their sleep. Overall, we can conclude that sleep in the social phenotype of individuals with RTT is related to progressive sensorimotor impairments. Therefore, in the future, the pathophysiology of the sensorimotor system should receive more attention in the study of sleep and the social life of individuals with RTT. In addition, we look forward to furthering research demonstrating the effects of sensorimotor therapies on sleep and social impairments
Wantzen, Prany. „La mémoire chez l’adolescent avec autisme : électrophysiologie, cognition et prise en charge“. Thesis, Paris Sciences et Lettres (ComUE), 2019. http://www.theses.fr/2019PSLEP071.
Der volle Inhalt der QuelleAutism spectrum disorders (ASD) are neurodevelopmental disorders, characterized by difficulties in social communication with restricted and repetitive behaviors. ASD are associated with structural, functional and connectivity brain abnormalities that contribute to atypical cognitive functioning in this population. This work includes three projects aimed at characterizing the neurocognitive profile of ASD adolescents and young adults and proposing new rehabilitation programs. The first shows abnormal resting-state brain connectivity using electroencephalography that can account for the multimodal integration difficulties that directly impact introspection processes. The second project deepens the study of introspection processes in the context of autobiographical memory (ABM). The data collected confirm the ABM difficulties in ASD adolescents, with an atypical sensory profile, but also the existence of a positive effect of prompting and visual cues during recall. Beyond, our work highlights the importance of ABM rehabilitation, used as a key vector in social interactions. Then, the third project concerns the creation of an ABM rehabilitation program based on an individual and collective approach. Preliminary results show a beneficial effect on the social identity of adolescents with autism. ABM is, therefore, very relevant to study in autism, integrating a unique and ecological multimodal dimension, and an interesting tool of rehabilitation
Mouaffak, Fayçal. „Schizophrénie Ultra Résistante : un trouble neurodéveloppemental : caractérisation clinique et génétique“. Paris 6, 2011. http://www.theses.fr/2011PA066725.
Der volle Inhalt der QuelleHerzine, Ameziane. „Etudes des effets neurodéveloppementaux induits par l’exposition périnatale à un pesticide, le glufosinate d’ammonium : de la neurogenèse au comportement“. Thesis, Orléans, 2016. http://www.theses.fr/2016ORLE2008/document.
Der volle Inhalt der QuelleGlufosinate ammonium (GLA) is one of the most widely used herbicides in agriculture. As for almost all pesticides, potential adverse effects of GLA have not been investigated in the brain developmental neurotoxicity perspective. Indeed, early pesticides exposure may weaken the developing brain and cause permanent brain alteration which could lead to a wide range of the lifelong effects on health and/or behavior. As an illustration, we showed that perinatal exposure to low doses of GLA induced behavioral defects in mice adulthood, characterized by many similarities with Autism Spectrum Disorders phenotype. My thesis deals with the molecular aspect of this perinatal GLA exposure. I demonstrated that GLA induced disturbances of proliferation and neuroblast migration from the subventricular zone to the olfactory bulbs. These defects were associated with significant change in the expression of many genes involved in neuroblast migration and cytoskeleton regulation as observed by brain transcriptome analysis. I showed that GLA act on the cytoskeleton through modification of polyglutamylation of tubulin which lead to cell division/migration disturbances and cell differentiation defect. My work thus provides a new molecular link between pre- and post-natal exposure to the herbicide GLA and the onset of ASD like phenotype later in life. It also raises the fundamental concerns about the ability of current safety testing to assess risks of pesticide exposure during critical developmental periods
Bücher zum Thema "Troubles du neurodéveloppement"
Maëva Roulin. Le diagnostic des troubles du neurodéveloppement chez l'adulte. Mardaga, 2021. http://dx.doi.org/10.14375/np.9782804720421.
Der volle Inhalt der QuelleBuchteile zum Thema "Troubles du neurodéveloppement"
Des Portes, Vincent. „D’une simple variante du développement du jeune enfant aux troubles du neurodéveloppement“. In Parentalité, développement, apprentissages, 113–40. Érès, 2020. http://dx.doi.org/10.3917/eres.suess.2020.01.0113.
Der volle Inhalt der QuelleGermanaud, David. „Troubles du neurodéveloppement en contexte d’exposition prénatale à l’alcool ou autres produits psychotropes“. In Santé et épanouissement de l’enfant : dans quel environnement ?, 107. ERES, 2018. http://dx.doi.org/10.3917/eres.bonne.2018.01.0107.
Der volle Inhalt der QuelleSperanza, Mario, Anne Revah-Levy, Alexandra Pham-Scottez, Corinne Dugré-Le Bigre und Maurice Corcos. „Chapitre 7. Identification d’un sous-type neurodéveloppemental de trouble de la personnalité borderline“. In Troubles de la personnalité borderline à l'adolescence, 85–99. Dunod, 2013. http://dx.doi.org/10.3917/dunod.corco.2013.02.0085.
Der volle Inhalt der QuelleBange, François. „Chapitre 1. Évolution nosographique de l’instabilité psychomotrice au trouble neurodéveloppemental“. In Trouble Déficit de l'Attention avec ou sans Hyperactivité de l'enfant à l'adulte, 6–24. Dunod, 2016. http://dx.doi.org/10.3917/dunod.bouva.2016.01.0006.
Der volle Inhalt der QuelleOuss, Lisa. „Autisme et maladie d’Alzheimer, du trouble neurodéveloppemental à la pathologie neurodégénérative : une lecture qui rende compte de la diversité des expressions cliniques“. In Et si Alzheimer(s) et Autisme(s) avaient un lien ?, 17–36. Érès, 2018. http://dx.doi.org/10.3917/eres.berge.2018.01.0017.
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