Liu Xin-Jun, Wei Jun, Shang Ying-Hui, Huang Han-Chang, Lao Feng-Xue
Beijing Key Laboratory of Bioactive Substances and Functional Foods, Beijing Union University, Beijing, P.R. China.
College of Arts and Science of Beijing Union University, Beijing, P.R. China.
J Alzheimers Dis. 2017;57(4):1157-1170. doi: 10.3233/JAD-161111.
Alzheimer's disease (AD) is a dementia disease with neuronal loss and synaptic impairment. This impairment is caused, at least partly, by the generation of two main AD hallmarks, namely the hyperphosphorylated tau protein comprising neurofibrillary tangles and senile plaques containing amyloid-β (Aβ) peptides. The amyloid-β protein precursor (AβPP) and glycogen synthase kinase-3β (GSK3β) are two main proteins associated with AD and are closely correlated with these hallmarks. Recently, both of the proteins were reported to be modulated by endoplasmic reticulum stress (ERS) and are involved in the pathogenesis of AD. The mechanism of ERS plus the modulation of AβPP processing and GSK3β activity by ERS in AD are summarized and explored in this review.
阿尔茨海默病（AD）是一种伴有神经元丧失和突触损伤的痴呆症。这种损伤至少部分是由两种主要的AD标志性病变引起的，即构成神经原纤维缠结的过度磷酸化tau蛋白和含有β淀粉样蛋白（Aβ）肽的老年斑。β淀粉样蛋白前体（AβPP）和糖原合酶激酶-3β（GSK3β）是与AD相关的两种主要蛋白质，并且与这些标志性病变密切相关。最近，有报道称这两种蛋白质都受到内质网应激（ERS）的调节，并参与AD的发病机制。本文综述并探讨了ERS的机制以及ERS对AD中AβPP加工和GSK3β活性的调节作用。
