Academic literature on the topic 'Maladie d'Alzheimer – étiologie'
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Dissertations / Theses on the topic "Maladie d'Alzheimer – étiologie":
Bui, Solange. "La maladie d'Alzheimer : aspects cliniques-histopathologie-hypothèses pathogéniques." Paris 5, 1992. http://www.theses.fr/1992PA05P059.
Wavrant-de-Vrieze, Fabienne. "Identification de nouveaux locus dans les formes tardives de la maladie d'Alzheimer." Lille 1, 1999. https://pepite-depot.univ-lille.fr/LIBRE/Th_Num/1999/50376-1999-417.pdf.
Lopez-Perez, Elvira. "La voie α-sécrétase de maturation de la protéine précurseur du peptide β-amyloi͏̈de dans la maladie d'Alzheimer : activités protéolytiques et régulation." Nice, 2000. http://www.theses.fr/2000NICE5459.
Le, Prince Ghislaine. "Intéractions neuroastrocytaires au cours du développement et de l'astrogliose réactionnelle, et dans la maladie d'Alzheimer." Paris 12, 1992. http://www.theses.fr/1992PA120048.
Da, Costa Emilie. "Synthèse d'huprines marquées au fluor-18 pour l'imagerie TEP de l'acétylcholinestérase et le suivi de la maladie d'Alzheimer." Chimie organique, bioorganique : réactivité et analyse (Mont-Saint-Aignan, Seine-Maritime ; 1996-....), 2013. http://www.theses.fr/2013ROUES045.
Gantier, René. "Analyse structurale et fonctionnelle des mutations de la préséniline 1 dans les formes autosomiques dominantes de la maladie d'Alzheimer." Rouen, 2000. http://www.theses.fr/2000ROUES014.
Gagliardi, Geoffroy. "Troubles positifs de la mémoire épisodique dans la maladie d'Alzheimer, du stade préclinique à la démence." Thesis, Sorbonne université, 2019. http://www.theses.fr/2019SORUS541.
Alzheimer’s Disease (AD) is a neurodegenerative pathology defined by the com- bination of progressive behavioral syndrome and specific brain damage. In recent decades, many therapeutic trials have been undertaken. Although some treatments can reduce the number of lesions or slow down cognitive development, no curative treatment has yet been developed. One of the main hypotheses of these failures is that treatments would be delivered too late, at a time when they would already have caused irreversible biological damage. Thus, a significant amount of research currently focuses on describing the preclinical stages of AD and determining the indicators (both behavioral and biological) that could predict a subsequent diagnosis. In this work, we try to establish cognitive measures that best describe this early stage in the evolution of AD. We focus particularly on memory, which is particularly involved in the phenotype of AD. A first part of this work focuses on post-diagnosis AD, highlighting the presence of links between memory errors and cognitive and biological aspects. In the second part, we demonstrate that these same relationships are present at a preclinical stage of the pathology, when patients present a subtle cognitive decline. Finally, our work highlights a link between the biological damage characteristic of AD and a lack of awareness of memory disorders
Bauer, Virginie. "Contribution à l'influence des événements de vie dans l'étiologie des maladies démentielles de l'âgé." Thesis, Université de Lorraine, 2012. http://www.theses.fr/2012LORR0339/document.
Among the elderly, Alzheimer disease and related pathologies currently constitute a real public health issue. The anatomo-pathological lesions of these diseases may be clearly defined but their etiology remains uncertain and is likely multifactorial. As a clinician psychologist, theories involving psychism in the etiology of demential diseases among elderly, first held my attention. A review of the question enabled me to make a list supposed to be exhaustive and divided into 3 categories : psycho-dynamic, psycho-social theories and multifactorial integrative patterns. Among the latter, the one involving life events as risk factors motivated this double research. Thus is a qualitive procedure, 2 studies started in parallel. The first retrospective dealing with life stories of a population of 30 people affected by Alzheimer or related diseases, hosted in a protected life-unit ; the second prospective scanning through cognitive evolution based on several years for 30 elderly people unharmed by troubles at the start of the study (depending on their life stories having many or few life events). If a certain amount of disturbing events are recounted by relatives for most of the patients of the retrospective research, the prospective research shows that an important number of live events is neither a sufficient nor a necessary condition to represent a risk factor of cognitive troubles. On the other hand, the elaboration or non elaboration of there events, their traumatic or non traumatic aspect (linked with the received or not received support and help) seems to be determining in the cognitive evolution of the subjects. Finally, among most of the subjects for whom past events prove to be traumatic, a contemporary "loss"-like episode would revive memories and would be an accelerating factor of cognitive troubles and even a collapse to a memory pathology
Gauvrit, Thibaut. "Conséquences d'un régime maternel riche en graisse durant la lactation chez la descendance dans un modèle murin de tauopathie." Electronic Thesis or Diss., Université de Lille (2022-....), 2024. https://pepite-depot.univ-lille.fr/ToutIDP/EDBSL/2024/2024ULILS006.pdf.
Numerous studies indicate that disruption of the perinatal environment contributes to the development of diseases in adult offspring. The most studied disturbance is malnutrition, which affects over 2 billion people worldwide. Studies have associated maternal malnutrition with short- and long-term alterations in offspring, particularly an increase in metabolic and cognitive disorders. Although most studies have focused on consequences at the peripheral level, a few have shown effects on the brain, which develops mainly during lactation in mice and late pregnancy in humans. Indeed, research suggests that a high-fat (HF) diet during the perinatal period causes alterations in the hippocampus (a structure essential to cognitive processes). Moreover, since metabolic alterations are a risk factor for Alzheimer's disease (AD), and cognitive impairment is a characteristic feature of the disease, it seems possible that maternal malnutrition may contribute to the development of AD. To date, few data are available, and no studies have applied the diet solely during lactation. Furthermore, no work has investigated the presence of a possible sexual dimorphism, despite the fact that AD affects women more than men. Thus, the main objective of my thesis work was to identify the effects of a maternal HF diet during lactation in adult male and female offspring in a mouse model mimicking the Tau pathology of AD (THY-Tau22 mice). To achieve this objective, C57Bl6/J females were crossed with THY-Tau22 males and subjected to a standard or HF (58% fat) diet during the 3-week lactation period. At weaning, THY-Tau22 offspring and their littermate were fed a standard diet until sacrifice at 4 (onset of Tau lesion) or 7 months of age (onset of cognitive decline). The results indicate that the HF maternal diet decreases maternal body weight during lactation and increases offspring body weight at weaning. In adulthood, the HF maternal diet induced glucose intolerance in male offspring only. The HF maternal diet also impaired spatial memory in male and female offspring, independently of genotype. In THY-Tau22 offspring, these disorders are accompanied by an increase in hippocampal Tau protein phosphorylation at 4 months of age in males and 7 months of age in females, highlighting a delay between the two sexes. Moreover, they are accompanied by an alteration in adult hippocampal neurogenesis, with increased proliferation in male C57Bl6/J offspring and mature neurons in female THY-Tau22 offspring. Furthermore, analyses reveal that the maternal HF diet modifies synapses, with a decrease in post-synaptic compartments in C57BL6/J females and in NR2B and SNAP25 proteins in THY-Tau22 males. Finally, using a multi-omics approach, we have shown that the maternal HF diet modifies the hippocampal transcriptome and proteome, affecting biological pathways associated with mitochondria, energy metabolism and translation, both in physiological and pathological conditions. However, the genes and proteins deregulated by maternal HF diet differ according to sex.Our data suggest that maternal malnutrition accelerates the onset of age-related alterations and tauopathy in offspring, and that its effects are sex-dependent. Our results confirm the importance of the perinatal environment as an opportune time for intervention in an attempt to stem the spread of metabolic and neurodegenerative diseases
Cruz, de Souza Leonardo. "La maladie d'Alzheimer : du diagnostic phénotypique au diagnostic étiologique." Paris 6, 2011. http://www.theses.fr/2011PA066410.