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雌激素通过通过ERββ调节IDO1-介导的Trp/Kyn代谢来调节APP/PS1雌性小鼠的认知功能

Lingdi Zhang¹, Shuang Hu², Jianjun Zhu¹

¹Department of Pharmacy, Affiliated Xiaoshan Hospital, Hangzhou Normal University, 311202, Hangzhou, China.

Hormones and behavior

|February 8, 2026

概括

雌激素缺乏会使阿尔茨海默氏症恶化.

科学领域:

神经科学是一个神经科学.
内分泌学在内分泌学.
免疫学免疫学免疫学

背景情况:

阿尔茨海默病 (AD) 不成比例地影响绝经后妇女,与雌激素缺乏有关.
印度列胺2,3-二氧化酶1 (IDO1) 酶活性影响神经炎症和认知功能.

研究的目的:

为了研究雌激素和IDO1在雌性小鼠中阿尔茨海默氏病的发病过程中的作用.
探索雌激素和IDO1抑制的治疗潜力.

主要方法:

利用APP/PS1转基因小鼠进行卵巢切除 (OVX),以模拟雌激素缺乏症.
服用雌激素 (E2),一种IDO1抑制剂 (1-MT) 和雌激素受体调节剂.
评估认知功能和测量IDO1,素 (Trp), kynurenine (Kyn) 途径代谢物和血清素 (5-HT) 的水平.

主要成果:

卵巢切除会加剧认知能力下降,并增加海马体的IDO1水平.
IDO1抑制和雌激素的使用改善了OVX小鼠的认知功能.
雌激素调节了Trp/Kyn通路和血清激素水平,其作用由ERβ介导.

结论:

雌激素缺乏通过增加IDO1活性,有助于女性患阿尔茨海默氏症的易感性.
雌激素替代疗法通过通过ERβ激活调节IDO1-三方通路,显示出治疗潜力.
针对IDO1或雌激素信号可能为绝经后妇女的阿尔茨海默氏症治疗提供新的策略.

关键词:

在APP/PS1小鼠中.阿尔茨海默病的疾病阿尔茨海默病的疾病.标签: 标签: IDO1 标签: IDO1 标签: IDO1 进行卵巢切除术.在Trp/Kyn路径上.

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