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Conference Paper: Alzheimer-like pathology in rat receiving passive smoking

TitleAlzheimer-like pathology in rat receiving passive smoking
Authors
KeywordsAlzheimer
Smoking
Beta-amyloid
Issue Date2009
PublisherSociety for Neuroscience.
Citation
Neuroscience 2009, Chicago, IL, 17-21 October 2009, Program#/Poster#: 626.13/H26 How to Cite?
AbstractAlthough epidemiological studies shows that smoking could increase the risk of Alzheimer’s disease (AD), the molecular basis linking smoking with increased incidence of AD is still unclear. We have established a model of passive smoking (1 hour per day exposure to either sham air or 4% cigarette smoke) for 8 weeks in the ventilated smoking chamber on Sprague-Dawley rats and investigated the changes of β-amyloid (Aβ) in the model. It was found that smoke exposure resulted in increased accumulation of Aβ, up-regulation of β amyloid precursor protein (APP), its proteolytic product sAPPβ fragment as well as β-site APP-cleaving enzyme 1 (BACE1). In addition, the level of nitrotyrosine, a marker of oxidative stress, and 8-hydroxyguanosine, a marker of oxidative damage, was found to be significantly increased in the hippocampus of passive smoking rats. Taken together, our data suggest that passive smoking can induce Alzheimer-like Aβ pathology, and this pathological event may be associated with increased oxidative stress. Our study provides compelling evidence to support the findings from epidemiological studies.
Persistent Identifierhttp://hdl.handle.net/10722/95182

 

DC FieldValueLanguage
dc.contributor.authorChang, RCCen_HK
dc.contributor.authorYang, Xen_HK
dc.contributor.authorHo, JYSen_HK
dc.contributor.authorYeung, SCen_HK
dc.contributor.authorMak, JCWen_HK
dc.date.accessioned2010-09-25T15:54:12Z-
dc.date.available2010-09-25T15:54:12Z-
dc.date.issued2009en_HK
dc.identifier.citationNeuroscience 2009, Chicago, IL, 17-21 October 2009, Program#/Poster#: 626.13/H26en_HK
dc.identifier.urihttp://hdl.handle.net/10722/95182-
dc.description.abstractAlthough epidemiological studies shows that smoking could increase the risk of Alzheimer’s disease (AD), the molecular basis linking smoking with increased incidence of AD is still unclear. We have established a model of passive smoking (1 hour per day exposure to either sham air or 4% cigarette smoke) for 8 weeks in the ventilated smoking chamber on Sprague-Dawley rats and investigated the changes of β-amyloid (Aβ) in the model. It was found that smoke exposure resulted in increased accumulation of Aβ, up-regulation of β amyloid precursor protein (APP), its proteolytic product sAPPβ fragment as well as β-site APP-cleaving enzyme 1 (BACE1). In addition, the level of nitrotyrosine, a marker of oxidative stress, and 8-hydroxyguanosine, a marker of oxidative damage, was found to be significantly increased in the hippocampus of passive smoking rats. Taken together, our data suggest that passive smoking can induce Alzheimer-like Aβ pathology, and this pathological event may be associated with increased oxidative stress. Our study provides compelling evidence to support the findings from epidemiological studies.-
dc.languageengen_HK
dc.publisherSociety for Neuroscience.-
dc.relation.ispartofSociety for Neuroscience Annual Meeting-
dc.rightsCopyright © Society for Neuroscience.-
dc.subjectAlzheimer-
dc.subjectSmoking-
dc.subjectBeta-amyloid-
dc.titleAlzheimer-like pathology in rat receiving passive smokingen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailChang, RCC: rccchang@hkucc.hku.hken_HK
dc.identifier.emailYang, X: yangxifeismile@yahoo.com.cnen_HK
dc.identifier.emailHo, JYS: janiceys@hku.hken_HK
dc.identifier.emailYeung, SC: flag@hku.hken_HK
dc.identifier.emailMak, JCW: judymak@hku.hk-
dc.identifier.authorityChang, RCC=rp00470en_HK
dc.identifier.authorityMak, JCW=rp00352en_HK
dc.identifier.hkuros168083en_HK
dc.publisher.placeWashington, DC-
dc.customcontrol.immutableyiu 150217-

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