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Article: Exploring ER Stress Response in Cellular Aging and Neuroinflammation in Alzheimer's Disease

TitleExploring ER Stress Response in Cellular Aging and Neuroinflammation in Alzheimer's Disease
Authors
KeywordsEndoplasmic reticulum
ER stress
Unfolded protein response
Aging
Alzheimer’s disease
Issue Date2021
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/arr
Citation
Ageing Research Reviews, 2021, v. 70, p. article no. 101417 How to Cite?
AbstractOne evident hallmark of Alzheimer’s disease (AD) is the irregular accumulation of proteins due to changes in proteostasis involving endoplasmic reticulum (ER) stress. To alleviate ER stress and reinstate proteostasis, cells undergo an integrated signaling cascade called the unfolded protein response (UPR) that reduces the number of misfolded proteins and inhibits abnormal protein accumulation. Aging is associated with changes in the expression of ER chaperones and folding enzymes, leading to the impairment of proteostasis and the accumulation of misfolded proteins. The disrupted initiation of UPR prevents the elimination of unfolded proteins, leading to ER stress. In AD, the accumulation of misfolded proteins caused by sustained cellular stress leads to neurodegeneration and neuronal death. Current research has revealed that ER stress can trigger an inflammatory response through diverse transducers of UPR. Although the involvement of a neuroinflammatory component in AD has been documented for decades, whether it is a contributing factor or part of the neurodegenerative events is so far unknown. Besides, a feedback loop occurs between neuroinflammation and ER stress, which is strongly associated with neurodegenerative processes in AD. In this review, we focus on the current research on ER stress and UPR in cellular aging and neuroinflammatory processes, leading to memory impairment and synapse dysfunction in AD.
Persistent Identifierhttp://hdl.handle.net/10722/301615
ISSN
2020 Impact Factor: 10.895
2020 SCImago Journal Rankings: 3.523

 

DC FieldValueLanguage
dc.contributor.authorUddin, MS-
dc.contributor.authorYU, WS-
dc.contributor.authorLim, LW-
dc.date.accessioned2021-08-09T03:41:39Z-
dc.date.available2021-08-09T03:41:39Z-
dc.date.issued2021-
dc.identifier.citationAgeing Research Reviews, 2021, v. 70, p. article no. 101417-
dc.identifier.issn1568-1637-
dc.identifier.urihttp://hdl.handle.net/10722/301615-
dc.description.abstractOne evident hallmark of Alzheimer’s disease (AD) is the irregular accumulation of proteins due to changes in proteostasis involving endoplasmic reticulum (ER) stress. To alleviate ER stress and reinstate proteostasis, cells undergo an integrated signaling cascade called the unfolded protein response (UPR) that reduces the number of misfolded proteins and inhibits abnormal protein accumulation. Aging is associated with changes in the expression of ER chaperones and folding enzymes, leading to the impairment of proteostasis and the accumulation of misfolded proteins. The disrupted initiation of UPR prevents the elimination of unfolded proteins, leading to ER stress. In AD, the accumulation of misfolded proteins caused by sustained cellular stress leads to neurodegeneration and neuronal death. Current research has revealed that ER stress can trigger an inflammatory response through diverse transducers of UPR. Although the involvement of a neuroinflammatory component in AD has been documented for decades, whether it is a contributing factor or part of the neurodegenerative events is so far unknown. Besides, a feedback loop occurs between neuroinflammation and ER stress, which is strongly associated with neurodegenerative processes in AD. In this review, we focus on the current research on ER stress and UPR in cellular aging and neuroinflammatory processes, leading to memory impairment and synapse dysfunction in AD.-
dc.languageeng-
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/arr-
dc.relation.ispartofAgeing Research Reviews-
dc.subjectEndoplasmic reticulum-
dc.subjectER stress-
dc.subjectUnfolded protein response-
dc.subjectAging-
dc.subjectAlzheimer’s disease-
dc.titleExploring ER Stress Response in Cellular Aging and Neuroinflammation in Alzheimer's Disease-
dc.typeArticle-
dc.identifier.emailLim, LW: limlw@hku.hk-
dc.identifier.authorityLim, LW=rp02088-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.arr.2021.101417-
dc.identifier.pmid34339860-
dc.identifier.scopuseid_2-s2.0-85111642020-
dc.identifier.hkuros324009-
dc.identifier.volume70-
dc.identifier.spagearticle no. 101417-
dc.identifier.epagearticle no. 101417-
dc.publisher.placeIreland-

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