钙
神经科学
神经退行性变
内质网
钙信号传导
细胞生物学
生物
程序性细胞死亡
转基因
体内
化学
疾病
信号转导
细胞凋亡
生物化学
内科学
医学
遗传学
基因
有机化学
作者
Kuan‐Chung Cheng,Chih‐Yuan Huang,Tsung‐Chi Hsieh,Hsueh‐Cheng Chiang
出处
期刊:Iubmb Life
[Wiley]
日期:2022-05-09
卷期号:74 (8): 754-762
被引量:1
摘要
Accumulated Aβ is one of the hallmarks of Alzheimer's disease. Although accumulated results from in vivo and in vitro studies have shown that accumulated Aβ causes learning and memory deficit, cell death, and lifespan reduction, the underlying mechanism remains elusive. In neurons, calcium dynamics is regulated by voltage-gated calcium channel (VGCC) and endoplasmic reticulum and is important for neuron survival and formation of learning and memory. The current study employs in vivo genetics to reveal the role of calcium regulation systems in Aβ-induced behavioral damage. Our data shows that although increased VGCC improves learning and memory in Aβ42 flies, reduction of VGCC and Inositol trisphosphate receptors extends Aβ42 flies' lifespan and improves cell viability. The complex role of calcium regulation systems in Aβ-induced damage suggests that the imbalance of calcium dynamic is one of the main factors to trigger learning and memory deficit and cell death in the disease.
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