File Download

There are no files associated with this item.

Supplementary

Conference Paper: Inositol 1,4,5-trisphosphate Receptor Modulators Protect Neurons Against Beta-amyloid Peptides (25-35 and 1-42)-induced Toxicity

TitleInositol 1,4,5-trisphosphate Receptor Modulators Protect Neurons Against Beta-amyloid Peptides (25-35 and 1-42)-induced Toxicity
Authors
KeywordsIP3 receptor
beta-amyloid
apoptosis
caspase
Issue Date2002
PublisherSociety for Neuroscience
Citation
Neuroscience 2002, Orlando, FL, 3-7 November 2002, Presentation no. 892.1 How to Cite?
AbstractBeta-amyloid (Aβ) peptides have been proposed to play important roles in the pathogenesis of Alzheimer’s disease. It is well known that Aβ peptides are toxic to neurons in vivo and in vitro. Recent studies have proposed that neuronal cell death induced by Aβ peptides could be due to its action on disrupting intracellular calcium homeostasis. In the present study, we aim to study the roles of IP3R in Aβ peptides neurotoxicity by using three IP3R modulators, FK506, 2-aminoethoxydiphenyl borate and Xestospongin C. Release of lactate dehydrogenase, visualization of apoptotic nuclei stained with 4',6'-diamidino-2-phenylindole (DAPI), PARP cleavage, and caspase-2 and caspase-3 activities were used to evaluated the toxic effects of Aβ peptides on primary cortical neurons. We found that all three IP3R modulators significantly attenuated Aβ peptides neurotoxicity, associated with the decrease of caspase-2 and caspase-3 activities. Taken together, these results reveal that IP3R plays important roles in Aβ peptides toxicity and could be an important pharmacological target in future therapeutic approaches. Supported by Hong Kong Research Grant Council (HKU 7305/00M) and The Molecular Institute of Technology for drug synthesis and discovery (AOE)
Persistent Identifierhttp://hdl.handle.net/10722/95330

 

DC FieldValueLanguage
dc.contributor.authorSuen, KCen_HK
dc.contributor.authorChang, RCCen_HK
dc.contributor.authorLin, KFen_HK
dc.contributor.authorHugon, Jen_HK
dc.date.accessioned2010-09-25T15:58:48Z-
dc.date.available2010-09-25T15:58:48Z-
dc.date.issued2002en_HK
dc.identifier.citationNeuroscience 2002, Orlando, FL, 3-7 November 2002, Presentation no. 892.1en_HK
dc.identifier.urihttp://hdl.handle.net/10722/95330-
dc.description.abstractBeta-amyloid (Aβ) peptides have been proposed to play important roles in the pathogenesis of Alzheimer’s disease. It is well known that Aβ peptides are toxic to neurons in vivo and in vitro. Recent studies have proposed that neuronal cell death induced by Aβ peptides could be due to its action on disrupting intracellular calcium homeostasis. In the present study, we aim to study the roles of IP3R in Aβ peptides neurotoxicity by using three IP3R modulators, FK506, 2-aminoethoxydiphenyl borate and Xestospongin C. Release of lactate dehydrogenase, visualization of apoptotic nuclei stained with 4',6'-diamidino-2-phenylindole (DAPI), PARP cleavage, and caspase-2 and caspase-3 activities were used to evaluated the toxic effects of Aβ peptides on primary cortical neurons. We found that all three IP3R modulators significantly attenuated Aβ peptides neurotoxicity, associated with the decrease of caspase-2 and caspase-3 activities. Taken together, these results reveal that IP3R plays important roles in Aβ peptides toxicity and could be an important pharmacological target in future therapeutic approaches. Supported by Hong Kong Research Grant Council (HKU 7305/00M) and The Molecular Institute of Technology for drug synthesis and discovery (AOE)-
dc.languageengen_HK
dc.publisherSociety for Neuroscience-
dc.relation.ispartofSociety for Neuroscience Annual Meetingen_HK
dc.subjectIP3 receptor-
dc.subjectbeta-amyloid-
dc.subjectapoptosis-
dc.subjectcaspase-
dc.titleInositol 1,4,5-trisphosphate Receptor Modulators Protect Neurons Against Beta-amyloid Peptides (25-35 and 1-42)-induced Toxicityen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailChang, RCC: rccchang@hkucc.hku.hken_HK
dc.identifier.emailHugon, J: jhugon@hkucc.hku.hken_HK
dc.identifier.authorityChang, RCC=rp00470en_HK
dc.identifier.hkuros74669en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats