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Conference Paper: Evaluation of endoplasmic reticulum stress in beta-amyloid peptide neurotoxicity

TitleEvaluation of endoplasmic reticulum stress in beta-amyloid peptide neurotoxicity
Authors
Issue Date2004
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neulet
Citation
The 23rd Scientific Meeting of the Hong Kong Society of Neurosciences. Hong Kong, 2004. In Neuroscience Letters, 2004, v. 370 n. supplement, p. S16 How to Cite?
AbstractOne of the pathological hallmarks of Alzheimer’s disease (AD) is the accumulation of beta-amyloid (A ) peptide in the senile plaques. Therefore, A neurotoxicity is believed to play significant roles in AD. Mutation of presenilin-1 (PS- 1) gene sensitizes neurons to A toxicity and causes dysfunctions of endoplasmic reticulum (ER). Thus, ER stress is considered to be involved in AD pathogenesis. In this study, we aim to investigate different signaling pathways for ER stress responses in A neurotoxicity. Neurons exposed to A peptide did not elicit induction of alternative splicing in Xbp-1 mRNA by IRE-1, up-regulation of Xbp-1 mRNA by ATF-6 and PERK phosphorylation. There were inductions of GRP 78 and GADD153 as well as activation of caspase-12 and caspase-7 after 16-h incubation of A peptide. The results suggested that ER stress is not an early event involved in A neurotoxicity. Activation of JNK and phosphorylation of eIF2 were found at early time-point. However, these signaling events and neuronal cell death were not mediated by ER stress responses. Taken together, ER stress seems to be a late response in A peptide-induced toxicity. Acknowledgements: This work is supported by HKU Seed Funding for Basic Research (202-2003) to RCCC and is a part for Area of Excellence (AoE/P-10/01).
Persistent Identifierhttp://hdl.handle.net/10722/67543
ISSN
2015 Impact Factor: 2.107
2015 SCImago Journal Rankings: 1.035

 

DC FieldValueLanguage
dc.contributor.authorYu, MSen_HK
dc.contributor.authorSuen, KCen_HK
dc.contributor.authorKwok, NSen_HK
dc.contributor.authorSo, KFen_HK
dc.contributor.authorChang, RCCen_HK
dc.date.accessioned2010-09-06T05:56:04Z-
dc.date.available2010-09-06T05:56:04Z-
dc.date.issued2004en_HK
dc.identifier.citationThe 23rd Scientific Meeting of the Hong Kong Society of Neurosciences. Hong Kong, 2004. In Neuroscience Letters, 2004, v. 370 n. supplement, p. S16en_HK
dc.identifier.issn0304-3940en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67543-
dc.description.abstractOne of the pathological hallmarks of Alzheimer’s disease (AD) is the accumulation of beta-amyloid (A ) peptide in the senile plaques. Therefore, A neurotoxicity is believed to play significant roles in AD. Mutation of presenilin-1 (PS- 1) gene sensitizes neurons to A toxicity and causes dysfunctions of endoplasmic reticulum (ER). Thus, ER stress is considered to be involved in AD pathogenesis. In this study, we aim to investigate different signaling pathways for ER stress responses in A neurotoxicity. Neurons exposed to A peptide did not elicit induction of alternative splicing in Xbp-1 mRNA by IRE-1, up-regulation of Xbp-1 mRNA by ATF-6 and PERK phosphorylation. There were inductions of GRP 78 and GADD153 as well as activation of caspase-12 and caspase-7 after 16-h incubation of A peptide. The results suggested that ER stress is not an early event involved in A neurotoxicity. Activation of JNK and phosphorylation of eIF2 were found at early time-point. However, these signaling events and neuronal cell death were not mediated by ER stress responses. Taken together, ER stress seems to be a late response in A peptide-induced toxicity. Acknowledgements: This work is supported by HKU Seed Funding for Basic Research (202-2003) to RCCC and is a part for Area of Excellence (AoE/P-10/01).-
dc.languageengen_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neuleten_HK
dc.relation.ispartofNeuroscience Lettersen_HK
dc.rightsNOTICE: this is the author’s version of a work that was accepted for publication in <Journal title>. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in PUBLICATION, [VOL#, ISSUE#, (DATE)] DOI#en_HK
dc.titleEvaluation of endoplasmic reticulum stress in beta-amyloid peptide neurotoxicityen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0304-3940&volume=370 supplement 1&spage=S16&epage=&date=2004&atitle=Evaluation+of+endoplasmic+reticulum+stress+in+beta-amyloid+peptide+neurotoxicityen_HK
dc.identifier.emailSo, KF: hrmaskf@hkucc.hku.hken_HK
dc.identifier.emailChang, RCC: rccchang@hkucc.hku.hken_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.identifier.authorityChang, RCC=rp00470en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.neulet.2004.09.001-
dc.identifier.hkuros96473en_HK
dc.identifier.volume370-
dc.identifier.issuesuppl.-
dc.identifier.spageS16-
dc.identifier.epageS16-
dc.publisher.placeIreland-
dc.description.otherThe 23rd Scientific Meeting of the Hong Kong Society of Neurosciences. Hong Kong, 2004. In Neuroscience Letters, 2004, v. 370 n. supplement, p. S16-

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