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Article: Cigarette smoking accelerated brain aging and induced pre-Alzheimer-like neuropathology in rats
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TitleCigarette smoking accelerated brain aging and induced pre-Alzheimer-like neuropathology in rats
 
AuthorsHo, YS2
Yang, X3
Yeung, SC1
Chiu, K2
Lau, CF2
Tsang, AWT2
Mak, JCW2 1
Chang, RCC2
 
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
 
CitationPLoS ONE, 2012, v. 7 n. 5, article no. e36752 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0036752
 
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.
 
ISSN1932-6203
2012 Impact Factor: 3.73
2012 SCImago Journal Rankings: 1.512
 
DOIhttp://dx.doi.org/10.1371/journal.pone.0036752
 
PubMed Central IDPMC3350465
 
ISI Accession Number IDWOS:000305338200040
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.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorHo, YS
 
dc.contributor.authorYang, X
 
dc.contributor.authorYeung, SC
 
dc.contributor.authorChiu, K
 
dc.contributor.authorLau, CF
 
dc.contributor.authorTsang, AWT
 
dc.contributor.authorMak, JCW
 
dc.contributor.authorChang, RCC
 
dc.date.accessioned2012-06-26T05:58:42Z
 
dc.date.available2012-06-26T05:58:42Z
 
dc.date.issued2012
 
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.
 
dc.description.naturepublished_or_final_version
 
dc.identifier.citationPLoS ONE, 2012, v. 7 n. 5, article no. e36752 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0036752
 
dc.identifier.doihttp://dx.doi.org/10.1371/journal.pone.0036752
 
dc.identifier.eissn1932-6203
 
dc.identifier.hkuros200046
 
dc.identifier.isiWOS:000305338200040
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.

 
dc.identifier.issn1932-6203
2012 Impact Factor: 3.73
2012 SCImago Journal Rankings: 1.512
 
dc.identifier.issue5, article no. e36752
 
dc.identifier.pmcidPMC3350465
 
dc.identifier.pmid22606286
 
dc.identifier.scopuseid_2-s2.0-84861003588
 
dc.identifier.urihttp://hdl.handle.net/10722/149789
 
dc.identifier.volume7
 
dc.languageeng
 
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
dc.publisher.placeUnited States
 
dc.relation.ispartofPLoS ONE
 
dc.relation.referencesReferences in Scopus
 
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 rats
 
dc.typeArticle
 
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<contributor.author>Lau, CF</contributor.author>
<contributor.author>Tsang, AWT</contributor.author>
<contributor.author>Mak, JCW</contributor.author>
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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