Abstract
Alzheimer’s disease (AD) is the most common neurodegenerative disease, characterized by progressive cognitive impairment and memory loss. So far, the pathogenesis of AD has not been fully understood. Research have shown that endoplasmic reticulum (ER) stress and unfolded protein response (UPR) participate in the occurrence and development of AD. Furthermore, various studies, both in vivo and in vitro, have shown that targeting ER stress and ER stress-mediated apoptosis contribute to the recovery of AD. Thus, targeting ER stress and ER stress-mediated apoptosis may be effective for treating AD. In this review, the molecular mechanism of ER stress and ER stress-mediated apoptosis, as well as the therapeutic effects of some natural compounds and small molecule inhibitors targeting ER stress and ER stress-mediated apoptosis in AD will be introduced.
Highlights
The endoplasmic reticulum (ER) is a crucial organelle of eukaryotic cells, whose functions include protein synthesis and folding, lipid biogenesis and calcium metabolism (Schwarz and Blower, 2016)
Under chronic or excessive ER stress, unfolded protein response (UPR) fails to maintain the homeostasis of ER, the apoptosis signaling pathway is activated, leading to a variety of diseases, including Alzheimer’s disease (AD) (Uddin et al, 2020)
Under chronic or excessive ER stress, UPR fails to maintain the homeostasis of ER, the apoptosis signaling pathways are activated, even resulting in cell death (Senft and Ronai, 2015; Iurlaro and Munoz-Pinedo, 2016)
Summary
The endoplasmic reticulum (ER) is a crucial organelle of eukaryotic cells, whose functions include protein synthesis and folding, lipid biogenesis and calcium metabolism (Schwarz and Blower, 2016). Under chronic or excessive ER stress, UPR fails to maintain the homeostasis of ER, the apoptosis signaling pathway is activated, leading to a variety of diseases, including Alzheimer’s disease (AD) (Uddin et al, 2020). Under chronic or excessive ER stress, UPR fails to maintain the homeostasis of ER, the apoptosis signaling pathways are activated, even resulting in cell death (Senft and Ronai, 2015; Iurlaro and Munoz-Pinedo, 2016).
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