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Chronic cerebral hypoperfusion in a mouse model of Alzheimer's disease: an additional contributing factor of cognitive impairment

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dc.contributor.authorLee, JS-
dc.contributor.authorIm, DS-
dc.contributor.authorAn, YS-
dc.contributor.authorHong, JM-
dc.contributor.authorGwag, BJ-
dc.contributor.authorJoo, IS-
dc.date.accessioned2012-03-28T06:09:54Z-
dc.date.available2012-03-28T06:09:54Z-
dc.date.issued2011-
dc.identifier.issn0304-3940-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/6347-
dc.description.abstractThe purpose of the present study was to evaluate whether chronic cerebral hypoperfusion would affect cognitive status in an Alzheimer mouse model. Behavioral tests and histological evaluations were performed using female Tg2576 mice eight weeks after right common carotid artery occlusion (rCCAO), which is known to induce a type of vascular dementia without neuronal necrosis in nontransgenic mice. Positron emission tomography with (18)F-fluorodeoxyglucose (FDG-PET) was utilized to evaluate metabolic status in the rCCAO-operated brain of nontransgenic mice. Escape latency from the Morris water maze test was not significantly different between rCCAO- and sham-operated mice. However, the learning curve was impaired in rCCAO-operated transgenic mice while it was preserved in sham-operated transgenic or rCCAO-operated nontransgenic mice. Histological examination revealed no evidence of cell death in the rCCAO-operated brains, and the extent of amyloid deposition was not different in rCCAO- and sham-operated mice. The brain of rCCAO-operated mice showed metabolic deficits in the ipsilateral parietal cortex through FDG-PET. In conclusion, further cognitive decline which is more comparable to typical Alzheimer's disease was induced by chronic cerebral hypoperfusion in an Alzheimer mouse model. This aggravation might be associated with hypometabolism via chronic cerebral hypoperfusion.-
dc.language.isoen-
dc.subject.MESHAlzheimer Disease-
dc.subject.MESHAnimals-
dc.subject.MESHBrain-
dc.subject.MESHBrain Ischemia-
dc.subject.MESHCarotid Stenosis-
dc.subject.MESHCerebrovascular Circulation-
dc.subject.MESHCognition Disorders-
dc.subject.MESHDementia, Vascular-
dc.subject.MESHFemale-
dc.subject.MESHGlucose-
dc.subject.MESHMaze Learning-
dc.subject.MESHMemory, Short-Term-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred C57BL-
dc.subject.MESHMice, Transgenic-
dc.subject.MESHSpecies Specificity-
dc.titleChronic cerebral hypoperfusion in a mouse model of Alzheimer's disease: an additional contributing factor of cognitive impairment-
dc.typeArticle-
dc.identifier.pmid21134418-
dc.identifier.urlhttp://linkinghub.elsevier.com/retrieve/pii/S0304-3940(10)01525-9-
dc.contributor.affiliatedAuthor이, 진수-
dc.contributor.affiliatedAuthor안, 영실-
dc.contributor.affiliatedAuthor홍, 지만-
dc.contributor.affiliatedAuthor곽, 병주-
dc.contributor.affiliatedAuthor주, 인수-
dc.type.localJournal Papers-
dc.identifier.doi10.1016/j.neulet.2010.11.071-
dc.citation.titleNeuroscience letters-
dc.citation.volume489-
dc.citation.number2-
dc.citation.date2011-
dc.citation.startPage84-
dc.citation.endPage88-
dc.identifier.bibliographicCitationNeuroscience letters, 489(2). : 84-88, 2011-
dc.identifier.eissn1872-7972-
dc.relation.journalidJ003043940-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Neurology
Journal Papers > School of Medicine / Graduate School of Medicine > Nuclear Medicine & Molecular Imaging
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
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