The abnormal deposition of amyloid-β peptide, a major component of senile plaques, has been reported to be the major cause of neuronal cell death and cognitive impairment in Alzheimer's disease (AD). Adult neurogenesis is related to the amelioration of impaired neurons and cognitive impairment. In the research, we investigated the function of curcumin on endogenous neural stem cells (NSCs) and hippocampal neurogenesis in mice. APP/PS1 transgenic mice as animal models were treated with curcumin, and a significant improvement in learning and memory function was observed. The improvement was associated with a significant increase in the number of new neural stem cells (BrdU+/Nestin+) and newborn neurons (NeuN/kI67+) in the hippocampal region and decreased the number of apoptotic neurons (TUNEL+ and Caspase-3/NeuN+). These results suggested that curcumin activated NSCs proliferation, improved neurogenesis, and ameliorated cognitive impairment of AD mice. Then, we identified that curcumin upregulated the expression of self-renewal genes, Notch1 and Hes1, and augmentation of CDK4, Cyclin D1, NICD, and Hes1 protein. As Notch activity was blocked by the DAPT, the related proteins were downregulated, and the initiating cell proliferation of curcumin was abolished. These results might suggest that the function of curcumin was dependent on Notch signaling pathway.

中文翻译：

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姜黄素通过Notch信号通路促进阿尔茨海默氏病小鼠中成年神经干细胞的增殖和神经元的诞生。

据报道，淀粉样蛋白-β肽（老年斑的主要成分）的异常沉积是阿尔茨海默病（AD）中神经元细胞死亡和认知障碍的主要原因。成人神经发生与神经元受损和认知障碍的改善有关。在研究中，我们研究了姜黄素对小鼠内源性神经干细胞（NSC）和海马神经发生的作用。用姜黄素处理APP / PS1转基因小鼠作为动物模型，并观察到其学习和记忆功能显着改善。这种改善与海马区新神经干细胞（BrdU + / Nestin +）和新生神经元（NeuN / kI67 +）的数量显着增加以及凋亡神经元的数量（TUNEL +和Caspase-3 / NeuN +）减少有关。这些结果表明姜黄素激活了NSC的增殖，改善了神经发生，并改善了AD小鼠的认知障碍。然后，我们发现姜黄素上调了自我更新基因Notch1和Hes1的表达，并上调了CDK4，Cyclin D1，NICD和Hes1蛋白。由于Notch活性被DAPT阻断，相关蛋白被下调，姜黄素的起始细胞增殖被取消。这些结果可能表明姜黄素的功能依赖于Notch信号通路。由于Notch活性被DAPT阻断，相关蛋白被下调，姜黄素的起始细胞增殖被取消。这些结果可能表明姜黄素的功能依赖于Notch信号通路。由于Notch活性被DAPT阻断，相关蛋白被下调，姜黄素的起始细胞增殖被取消。这些结果可能表明姜黄素的功能依赖于Notch信号通路。