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Implication du récepteur LSR (lipolysis stimulated lipoprotein receptor) dans le contrôle de l’homéostasie du cholestérol cérébral et les capacités cognitives au cours du vieillissement

Abstract : Alzheimer's disease (AD) is a neurodegenerative disease affecting millions of people. The origin of AD is multifactorial. Studies suggest that disturbance of cholesterol metabolism contributes to AD development. However, data in the literature is conflicting. It is therefore crucial to better characterize the metabolism and involvement of cholesterol in AD. This work focused on the Lipolysis Stimulated Lipoprotein Receptor (LSR), a hepatic lipoprotein receptor involved in the clearance of lipoproteins during the postprandial phase. The objectives of this thesis were to characterize LSR receptor expression profile in the mouse brain, and to determine its role in both brain cholesterol homeostasis and in the pathophysiology of AD. We identified and characterized LSR expression in brain structures that are involved in cognitive abilities and the regulation of energy metabolism. Next, using a mouse model heterozygous for the LSR receptor, we were able to demonstrate that the deletion of one allele LSR causes impaired brain cholesterol metabolism in aging, which was correlated with increased susceptibility to amyloid stress. These results suggest a role of LSR receptor in brain cholesterol homeostasis and show that alterations of the brain cholesterol metabolism can impact AD pathophysiology. Finally, we observed that the deficiency of an LSR allele in mice on a high fat diets affected peripheral lipid metabolism and the anxiety in these mice
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Submitted on : Thursday, March 29, 2018 - 1:01:17 PM
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  • HAL Id : tel-01751001, version 1

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Anthony Pinçon. Implication du récepteur LSR (lipolysis stimulated lipoprotein receptor) dans le contrôle de l’homéostasie du cholestérol cérébral et les capacités cognitives au cours du vieillissement. Médecine humaine et pathologie. Université de Lorraine, 2014. Français. ⟨NNT : 2014LORR0141⟩. ⟨tel-01751001⟩

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