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Article: Cigarette smoking accelerated brain aging and induced pre-Alzheimer-like neuropathology in rats

TitleCigarette smoking accelerated brain aging and induced pre-Alzheimer-like neuropathology in rats
Authors
KeywordsAlzheimer disease
Animal experiment
Cigarette smoking
Cytoskeleton
Dentate gyrus
Issue Date2012
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
PLoS ONE, 2012, v. 7 n. 5, article no. e36752 How to Cite?
Abstract
Cigarette smoking has been proposed as a major risk factor for aging-related pathological changes and Alzheimer's disease (AD). To date, little is known for how smoking can predispose our brains to dementia or cognitive impairment. This study aimed to investigate the cigarette smoke-induced pathological changes in brains. Male Sprague-Dawley (SD) rats were exposed to either sham air or 4% cigarette smoke 1 hour per day for 8 weeks in a ventilated smoking chamber to mimic the situation of chronic passive smoking. We found that the levels of oxidative stress were significantly increased in the hippocampus of the smoking group. Smoking also affected the synapse through reducing the expression of pre-synaptic proteins including synaptophysin and synapsin-1, while there were no changes in the expression of postsynaptic protein PSD95. Decreased levels of acetylated-tubulin and increased levels of phosphorylated-tau at 231, 205 and 404 epitopes were also observed in the hippocampus of the smoking rats. These results suggested that axonal transport machinery might be impaired, and the stability of cytoskeleton might be affected by smoking. Moreover, smoking affected amyloid precursor protein (APP) processing by increasing the production of sAPPbeta and accumulation of beta-amyloid peptide in the CA3 and dentate gyrus region. In summary, our data suggested that chronic cigarette smoking could induce synaptic changes and other neuropathological alterations. These changes might serve as evidence of early phases of neurodegeneration and may explain why smoking can predispose brains to AD and dementia.
Persistent Identifierhttp://hdl.handle.net/10722/149789
ISSN
2013 Impact Factor: 3.534
2013 SCImago Journal Rankings: 1.724
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
HKU (University of Hong Kong) Alzheimer's Disease Research Network under Strategic Research Theme on Healthy AgingGRF 761609M
NSFC/RGC70707M
Seed Funding for Basic Science Research201011159058
Small Grant Research201007176112
Funding Information:

Sources of funding support include: HKU (University of Hong Kong) Alzheimer's Disease Research Network under Strategic Research Theme on Healthy Aging, GRF 761609M & NSFC/RGC70707M, Seed Funding for Basic Science Research (201011159058) to RCCC, Small Grant Research (201007176112) to YSH. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

References

 

Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine
  2. The University of Hong Kong
  3. Shenzhen Centre of Disease Control and Prevention
DC FieldValueLanguage
dc.contributor.authorHo, YSen_US
dc.contributor.authorYang, Xen_US
dc.contributor.authorYeung, SCen_US
dc.contributor.authorChiu, Ken_US
dc.contributor.authorLau, CFen_US
dc.contributor.authorTsang, AWTen_US
dc.contributor.authorMak, JCWen_US
dc.contributor.authorChang, RCCen_US
dc.date.accessioned2012-06-26T05:58:42Z-
dc.date.available2012-06-26T05:58:42Z-
dc.date.issued2012en_US
dc.identifier.citationPLoS ONE, 2012, v. 7 n. 5, article no. e36752en_US
dc.identifier.issn1932-6203en_US
dc.identifier.urihttp://hdl.handle.net/10722/149789-
dc.description.abstractCigarette smoking has been proposed as a major risk factor for aging-related pathological changes and Alzheimer's disease (AD). To date, little is known for how smoking can predispose our brains to dementia or cognitive impairment. This study aimed to investigate the cigarette smoke-induced pathological changes in brains. Male Sprague-Dawley (SD) rats were exposed to either sham air or 4% cigarette smoke 1 hour per day for 8 weeks in a ventilated smoking chamber to mimic the situation of chronic passive smoking. We found that the levels of oxidative stress were significantly increased in the hippocampus of the smoking group. Smoking also affected the synapse through reducing the expression of pre-synaptic proteins including synaptophysin and synapsin-1, while there were no changes in the expression of postsynaptic protein PSD95. Decreased levels of acetylated-tubulin and increased levels of phosphorylated-tau at 231, 205 and 404 epitopes were also observed in the hippocampus of the smoking rats. These results suggested that axonal transport machinery might be impaired, and the stability of cytoskeleton might be affected by smoking. Moreover, smoking affected amyloid precursor protein (APP) processing by increasing the production of sAPPbeta and accumulation of beta-amyloid peptide in the CA3 and dentate gyrus region. In summary, our data suggested that chronic cigarette smoking could induce synaptic changes and other neuropathological alterations. These changes might serve as evidence of early phases of neurodegeneration and may explain why smoking can predispose brains to AD and dementia.en_US
dc.languageengen_US
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_US
dc.relation.ispartofPLoS ONEen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectAlzheimer disease-
dc.subjectAnimal experiment-
dc.subjectCigarette smoking-
dc.subjectCytoskeleton-
dc.subjectDentate gyrus-
dc.titleCigarette smoking accelerated brain aging and induced pre-Alzheimer-like neuropathology in ratsen_US
dc.typeArticleen_US
dc.identifier.emailHo, YS: janiceys@hku.hken_US
dc.identifier.emailYeung, SC: flag@hkucc.hku.hken_US
dc.identifier.emailChiu, K: datwai@hkucc.hku.hk-
dc.identifier.emailLau, CF: jefferyl@hkucc.hku.hk-
dc.identifier.emailTsang, AWT: andreat@hku.hk-
dc.identifier.emailMak, JCW: judymak@hku.hk-
dc.identifier.emailChang, RCC: rccchang@hku.hk-
dc.identifier.authorityMak, JCW=rp00352en_US
dc.identifier.authorityChang, RCC=rp00470en_US
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1371/journal.pone.0036752en_US
dc.identifier.pmid22606286-
dc.identifier.pmcidPMC3350465-
dc.identifier.scopuseid_2-s2.0-84861003588en_US
dc.identifier.hkuros200046-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84861003588&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume7en_US
dc.identifier.issue5, article no. e36752en_US
dc.identifier.eissn1932-6203-
dc.identifier.isiWOS:000305338200040-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridChang, RCC=7403713410en_US
dc.identifier.scopusauthoridMak, JCW=7103323094en_US
dc.identifier.scopusauthoridTsang, AWT=55216827400en_US
dc.identifier.scopusauthoridLau, CF=25122803900en_US
dc.identifier.scopusauthoridChiu, K=15076970500en_US
dc.identifier.scopusauthoridYeung, SC=25923636600en_US
dc.identifier.scopusauthoridYang, X=35622658300en_US
dc.identifier.scopusauthoridHo, YS=14031513600en_US

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