Modulation of AβPP and GSK3β by Endoplasmic Reticulum Stress and Involvement in Alzheimer’s Disease

Article type: Review Article

Authors: Liu, Xin-jun^{a; b} | Wei, Jun^{a; b} | Shang, Ying-hui^{a; b} | Huang, Han-chang^{a; b} | Lao, Feng-xue^{a; b; *}

Affiliations: [a] Beijing Key Laboratory of Bioactive Substances and Functional Foods, Beijing Union University, Beijing, P.R. China | [b] College of Arts and Science of Beijing Union University, Beijing, P.R. China

Correspondence: [*] Correspondence to: Feng-xue Lao, Beijing Key Laboratory of Bioactive Substances and Functional Foods, Beijing Union University; College of Arts and Science of Beijing Union University, Beijing 100191, P.R. China. Tel.: +86 10 62004513; E-mail: [email protected].

Abstract: 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.

Keywords: Alzheimer’s disease, amyloid-β, apoptosis, endoplasmic reticulum stress, neurofibrillary tangles

DOI: 10.3233/JAD-161111

Journal: Journal of Alzheimer's Disease, vol. 57, no. 4, pp. 1157-1170, 2017