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卵巢切除术和高脂肪高糖高盐饮食诱导的小鼠阿尔茨海默病/血管性痴呆特征。

Ovariectomy and High Fat-Sugar-Salt Diet Induced Alzheimer's Disease/Vascular Dementia Features in Mice.

机构信息

Department of Neurology, The Agnes Ginges Center for Human Neurogenetics, Hadassah Hebrew University Medical Center, Jerusalem, Israel.

Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel. Hadassah BrainLabs-National Knowledge Center for Research on Brain Diseases, Hadassah-Hebrew University Medical Center, Jerusalem Israel.

出版信息

Aging Dis. 2024 Oct 1;15(5):2284-2300. doi: 10.14336/AD.2024.03110.

Abstract

While the vast majority of Alzheimer's disease (AD) is non-familial, the animal models of AD that are commonly used for studying disease pathogenesis and development of therapy are mostly of a familial form. We aimed to generate a model reminiscent of the etiologies related to the common late-onset Alzheimer's disease (LOAD) sporadic disease that will recapitulate AD/dementia features. Naïve female mice underwent ovariectomy (OVX) to accelerate aging/menopause and were fed a high fat-sugar-salt diet to expose them to factors associated with increased risk of development of dementia/AD. The OVX mice fed a high fat-sugar-salt diet responded by dysregulation of glucose/insulin, lipid, and liver function homeostasis and increased body weight with slightly increased blood pressure. These mice developed AD-brain pathology (amyloid and tangle pathologies), gliosis (increased burden of astrocytes and activated microglia), impaied blood vessel density and neoangiogenesis, with cognitive impairment. Thus, OVX mice fed on a high fat-sugar-salt diet imitate a non-familial sporadic/environmental form of AD/dementia with vascular damage. This model is reminiscent of the etiologies related to the LOAD sporadic disease that represents a high portion of AD patients, with an added value of presenting concomitantly AD and vascular pathology, which is a common condition in dementia. Our model can, thereby, provide a valuable tool for studying disease pathogenesis and for the development of therapeutic approaches.

摘要

虽然绝大多数阿尔茨海默病(AD)是非家族性的,但用于研究疾病发病机制和治疗方法开发的 AD 动物模型大多为家族性形式。我们旨在生成一种类似于与常见的迟发性阿尔茨海默病(LOAD)散发性疾病相关的病因的模型,该模型将再现 AD/痴呆的特征。天真的雌性小鼠接受卵巢切除术(OVX)以加速衰老/绝经,并喂食高脂肪-高糖-高盐饮食,使其接触与痴呆/AD 发展风险增加相关的因素。接受高脂肪-高糖-高盐饮食的 OVX 小鼠通过葡萄糖/胰岛素、脂质和肝功能稳态失调以及体重增加(血压略有升高)来做出反应。这些小鼠出现 AD 脑病理(淀粉样蛋白和缠结病理)、神经胶质增生(星形胶质细胞和活化小胶质细胞负担增加)、血管密度和新生血管减少,伴有认知障碍。因此,接受高脂肪-高糖-高盐饮食的 OVX 小鼠模拟了一种非家族性散发性/环境形式的 AD/痴呆,伴有血管损伤。该模型类似于与 LOAD 散发性疾病相关的病因,该疾病代表了大量的 AD 患者,具有同时呈现 AD 和血管病理的附加价值,这是痴呆症的常见情况。因此,我们的模型可以为研究疾病发病机制和治疗方法的开发提供有价值的工具。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c99/11346392/f3f64c692405/AD-15-5-2284-g1.jpg

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