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基础科学和病原发生学

Miriam Bettinetti-Luque1, Laura Trujillo-Estrada1, Juana Andreo-Lopez1

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来自肥胖或糖尿病小鼠的内脏脂肪组织会使阿尔茨海默病 (AD) 的病理状况恶化. 这种恶化与免疫系统激活有关,这表明内脏脂肪是AD的治疗点.

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科学领域:

  • 神经科学是一个神经科学.
  • 代谢性疾病研究研究
  • 免疫学 免疫学 免疫学

背景情况:

  • 阿尔茨海默病 (AD) 涉及复杂的机制,代谢变化越来越多地与其进展有关.
  • 糖尿病和肥胖是已知的阿尔茨海默病的风险因素,与扩大的内脏脂肪组织有关.
  • 内脏脂肪组织可能会调解外周代谢功能障碍和大脑疾病之间的联系.

研究的目的:

  • 研究内脏脂肪组织在调解代谢功能障碍和阿尔茨海默病病理学的作用.
  • 为了确定从代谢受损状态的内脏脂肪组织是否会在AD模型中加剧tau病理和神经炎症.

主要方法:

  • 使用组织学和生物化学方法分析野生型 (WT),db/db (遗传肥胖/糖尿病) 和高脂肪饮食 (HFD) 养的WT小鼠的内脏脂肪组织.
  • 脂肪组织移植实验:db/db脂肪进入3xTg-AD小鼠和HFD养的WT脂肪进入Tau P301S小鼠.
  • 评估病理,p25/p35表达,IL-1β水平和微质激活.

主要成果:

  • 来自db/db捐赠者的内脏脂肪移植显著增加了3xTg-AD小鼠的tau病理,与增加的p25/p35,IL-1β和微质激活相关.
  • 同样,从高度养WT捐赠者的脂肪在Tau P301S小鼠中加剧了tau病理和神经炎症.
  • 这些发现表明,内脏脂肪组织的代谢功能障碍驱动神经炎症并加剧病理.

结论:

  • 来自代谢受损 (肥胖/糖尿病或饮食引起的肥胖) 的小鼠的内脏脂肪组织在AD模型中加剧了tau病理.
  • 这种恶化是通过免疫系统的激活发生的,突出显示了代谢障碍和AD之间的新型相互作用.
  • 内脏脂肪组织成为缓解AD进展的潜在治疗点.