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Analyse d’un nouveau modèle transgénique murin d’Alzheimer à début tardif basé sur la surexpression de BIN1 et induisant des endophénotypes précliniques de la maladie

Abstract : Late-onset Alzheimer’s Disease (LOAD) is the most common form of dementia and one of the most challenging disease of modern society. Although familial Alzheimer’s Disease (FAD) only account for 2% of the cases, research on the molecular basis of this pathology has mostly been performed on animal models of FAD. The first objective of this doctoral thesis was to identify new pathways involved in LOAD physiopathology. New synaptic partners of BIN1, the second most associated locus with LOAD after APOE, have been characterized. The second objective of this thesis was to study a new mouse model of LOAD, after APOE models: a mouse mimicking the overexpression of BIN1 found in patients. Together, the results place BIN1 in a synaptic interactome involved in the regulation of two major hallmarks of LOAD: dendritic spine morphology and amyloid β peptide regulation. They also link BIN1 with an alteration of the Lateral Entorhinal Cortex, which is the first brain structure affected in patients. Altogether, this doctoral thesis gives new insights on molecular pathways involved in early pathologic features of LOAD, at early presymptomatic stages of the disease, attainable by new therapeutic strategies.
Keywords : Neuroscience
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Theses
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https://tel.archives-ouvertes.fr/tel-01589667
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Submitted on : Monday, September 18, 2017 - 6:58:18 PM
Last modification on : Friday, March 27, 2020 - 2:22:57 AM

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Rachel Daudin. Analyse d’un nouveau modèle transgénique murin d’Alzheimer à début tardif basé sur la surexpression de BIN1 et induisant des endophénotypes précliniques de la maladie. Médecine humaine et pathologie. Université Sorbonne Paris Cité, 2016. Français. ⟨NNT : 2016USPCB034⟩. ⟨tel-01589667⟩

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