粒体自噬
莫里斯水上航行任务
开阔地
品脱1
帕金
氧化应激
下调和上调
胰岛素样生长因子
淀粉样前体蛋白
转基因小鼠
水迷宫
海马体
化学
内分泌学
内科学
转基因
生物
生长因子
医学
细胞凋亡
自噬
阿尔茨海默病
帕金森病
生物化学
受体
疾病
基因
作者
Ying Wang,Chaoyuan Song,Guoliang Yin,Meng Ye,Fengxia Zhang
出处
期刊:Brain Research
[Elsevier]
日期:2023-12-28
卷期号:1827: 148743-148743
被引量:1
标识
DOI:10.1016/j.brainres.2023.148743
摘要
By safeguarding the neurological system, insulin-like growth factor 1 (IGF-1) may have a role in the etiology of Alzheimer's disease (AD). The mechanism and signaling route, however, remain unclear. This research aimed to investigate the impact of IGF-1 on AD as well as its possible mechanism and signaling route. In this work, intracerebroventricular AAV9-IGF-1 was delivered to APP/PS1 transgenic mice. Following therapy, the Morris water maze and passive avoidance tests were administered to evaluate spatial learning and memory. The elevated plus maze, the open field test, and the sucrose preference test were used to evaluate anxious-depressive-like behavior. Thioflavin S staining was employed to visualize Aβ deposition, and ELISA was used to determine the quantities of soluble Aβ1-40 and Aβ1-42. Transmission electron microscopy was used to view the mitochondrial structure and mitophagy vesicles. The protein expression levels of PINK1, Parkin, and LC3-II/LC3-I were finally determined by Western blotting. AAV9-IGF-1 therapy enhanced spatial learning and memory, relieved anxious-depressive-like behavior impairments, lowered amyloid-β deposition, and decreased levels of soluble Aβ1-40 and Aβ1-42. In addition, AAV9-IGF-1 therapy restored mitochondrial integrity and increased the number of mitophagy in transgenic mice expressing APP/PS1. These results indicate that IGF-1 is protective for APP/PS1 mice. The mechanism of the favorable benefits mediated by IGF-1 was connected to an increase in mitophagy, which might give a novel therapy target in the future.
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