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Chronic stress accelerates learning and memory impairments and increases amyloid deposition in APPV717I-CT100 transgenic mice, an Alzheimer's disease model

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dc.contributor.authorJeong, Yun Ha-
dc.contributor.authorPark, Cheol Hyoung-
dc.contributor.authorYoo, Jongman-
dc.contributor.authorShin, Ki Young-
dc.contributor.authorAhn, Sung-Min-
dc.contributor.authorKim, Hye-Sun-
dc.contributor.authorLee, Sang Hyung-
dc.contributor.authorEmson, Piers C.-
dc.contributor.authorSuh, Yoo-Hun-
dc.date.accessioned2010-01-06T02:21:52Z-
dc.date.available2010-01-06T02:21:52Z-
dc.date.issued2006-02-10-
dc.identifier.citationFASEB J. 2006 Apr;20(6):729-31. Epub 2006 Feb 8.en
dc.identifier.issn1530-6860 (Electronic)-
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16467370-
dc.identifier.urihttps://hdl.handle.net/10371/25970-
dc.description.abstractAlthough chronic stress is known to be linked with memory and other neurological disorders, little is known about the relationship between chronic stress and the onset or development of Alzheimer's disease (AD). In this study, we investigated the effects of long-term stress on the onset and severity of cognitive deficits and pathological changes in APPV717I-CT100 mice overexpressing human APP-CT100 containing the London mutation (V717I) after exposure to immobilization stress. We found that chronic immobilization stress accelerated cognitive impairments, as accessed by the Passive avoidance and the Social Transfer of Food Preference (STFP) tests. Moreover, the numbers and densities of vascular and extracellular deposits containing amyloid beta peptide (Abeta) and carboxyl-terminal fragments of amyloid precursor protein (APP-CTFs), which are pathologic markers of AD, were significantly elevated in stressed animals, especially in the hippocampus. Moreover, stressed animals, also showed highly elevated levels of neurodegeneration and tau phosphorylation and increased intraneuronal Abeta and APP-CTFs immunoreactivities in the hippocampus and in the entorhinal and piriform cortex. This study provides the first evidence that chronic stress accelerates the onset and severity of cognitive deficits and that these are highly correlated with pathological changes, which thus indicates that chronic stress may be an important contributor to the onset and development of AD.en
dc.language.isoenen
dc.publisherFederation of American Society of Experimentalen
dc.subjectAlzheimer Disease/genetics/*metabolismen
dc.subjectAmyloid beta-Protein Precursor/genetics/*metabolismen
dc.subjectAnimalsen
dc.subjectCerebral Cortex/metabolismen
dc.subjectChronic Diseaseen
dc.subjectCorticosterone/blooden
dc.subjectDisease Models, Animalen
dc.subjectHippocampus/metabolismen
dc.subjectLearning Disorders/*metabolismen
dc.subjectMemory Disorders/*metabolismen
dc.subjectMiceen
dc.subjectMice, Transgenicen
dc.subjectRestraint, Physical/adverse effectsen
dc.subjectStress, Psychological/genetics/*metabolismen
dc.titleChronic stress accelerates learning and memory impairments and increases amyloid deposition in APPV717I-CT100 transgenic mice, an Alzheimer's disease modelen
dc.typeArticleen
dc.contributor.AlternativeAuthor정윤하-
dc.contributor.AlternativeAuthor박철형-
dc.contributor.AlternativeAuthor유종만-
dc.contributor.AlternativeAuthor신기영-
dc.contributor.AlternativeAuthor안성민-
dc.contributor.AlternativeAuthor김혜선-
dc.contributor.AlternativeAuthor이상형-
dc.contributor.AlternativeAuthor서유헌-
dc.identifier.doi10.1096/fj.05-4265fje-
Appears in Collections:
College of Medicine/School of Medicine (의과대학/대학원)Pharmacology (약리학전공)Journal Papers (저널논문_약리학전공)
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