阿尔茨海默病病理学和中年肥胖症的神经退行:一个试点研究
Mahsa Dolatshahi1, Paul K Commean1, Farzaneh Rahmani1
1Mallinckrodt Institute of Radiology, Washington University in St. Louis, St. Louis, Missouri, USA.
Aging and disease
|August 7, 2023
概括
中年肥胖,特别是内脏脂肪,与阿尔茨海默病 (AD) 风险增加有关. 较高的内脏脂肪与大脑变化和粉样蛋白积累相关,这表明在认知正常的成年人中早期的AD病理.
科学领域:
- 神经科学是一个神经科学.
- 放射学 放射学是一门学科.
- 代谢性疾病是一种代谢性疾病.
背景情况:
- 中年肥胖和内脏脂肪是阿尔茨海默病 (AD) 的危险因素.
- 内脏脂肪与胰岛素抵抗和炎症有关,这是AD病理学的关键机制.
- 在认知正常的个体中早期发现AD病理对于了解疾病进展至关重要.
研究的目的:
- 评估肥胖,腹部脂肪组织,胰岛素抵抗和早期阿尔茨海默病生物标志物 (粉样蛋白/蛋白吸收,大脑体积,皮层厚度) 之间的关联.
- 在一个认知正常的中年成年人队伍中调查这些关联.
- 探索内脏肥胖在临床前AD中的作用.
主要方法:
- 32名认知正常的中年成年人接受了血液检查,脑/腹部MRI和粉样蛋白/粉样蛋白PET扫描.
- 使用MRI量化了内脏和皮下脂肪组织 (VAT,SAT).
- 斯皮尔曼的部分相关性分析了脂肪标记物,胰岛素耐药性和PET/MRI衍生的大脑测量之间的关联.
主要成果:
- 较高的内脏和皮下脂肪组织 (VAT/SAT) 比率与右前皮质皮质粉样蛋白沉积增加相关,特别是在男性中.
- 增加的VAT/SAT比率和粉样蛋白吸收与AD特征大脑区域的皮质厚度降低有关.
- 较高的体重指数 (BMI) 和胰岛素抵抗与双边极皮质厚度下降有关.
结论:
- 在中年时代,内脏肥胖与前肌中较高的粉样蛋白病理有关.
- 内脏肥胖,胰岛素耐药性和粉样蛋白病理与AD标志区域的皮质厚度降低有关.
- 这些发现突显了代谢因素对正常认知的早期AD病理学的影响.
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