自噬
淀粉样前体蛋白
转基因小鼠
神经保护
细胞生物学
转基因
ATG5型
化学
淀粉样前体蛋白分泌酶
齿状回
程序性细胞死亡
ADAM10型
下调和上调
β淀粉样蛋白
BACE1-AS系列
阿尔茨海默病
细胞凋亡
神经科学
生物
酶
海马体
生物化学
内科学
疾病
医学
基因
金属蛋白酶
肽
去整合素
作者
Xiaoxue Du,Xue Huo,Yang Yang,Zhiying Hu,Benson O. A. Botchway,Yuting Jiang,Marong Fang
标识
DOI:10.1016/j.toxlet.2017.08.082
摘要
One role of BACE 1 (Beta-site amyloid precursor protein cleaving enzyme 1) is to cleave the sequential amyloid precursor protein (APP) into β-Amyloid (Aβ), the accumulation of which is an important participant in the formation of the amyloid plaques and neurofibrillary tangles of Alzheimer’s disease (AD). Our previous study showed BACE 1, the potential functional downstream target of miR-124, to be connected to cell death in AD cell models. Recent studies have shown that autophagy is altered in AD, however, as to whether miR-124 is involved in this alteration is not clear. In this study, 7-month-old APP/PS1 transgenic mice were transfected with miR-124 lentiviral vectors, injected bilaterally into the dentate gyrus (DG) of mice hippocampi. Following 7 days of recovery, both behavior and biochemical pathology tests were implemented. The results demonstrated learning ability improvement and specific AD pathology alleviation. Meanwhile there was down-regulation of Bcl-2 to Bax ratio expression, increase in Beclin-1 and decreases in expression of LC3II, Atg5 and p62/SQSTMl. In view of this, we hypothesis that miR-124 conducts its neuroprotective effect through BACE 1 by regulation of autophagic pathways.
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