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Plasma Carbonic Anhydrase II protein is Elevated in Alzheimer's Disease

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dc.contributor.authorJang, Bong Geom-
dc.contributor.authorYun, Sang-Moon-
dc.contributor.authorAhn, Kyungsook-
dc.contributor.authorSong, Ju Hee-
dc.contributor.authorJo, Sangmee A.-
dc.contributor.authorKim, Young-Yul-
dc.contributor.authorKim, Doh Kwan-
dc.contributor.authorPark, Moon Ho-
dc.contributor.authorHan, Changsu-
dc.contributor.authorKoh, Young Ho-
dc.date.accessioned2021-09-08T10:19:03Z-
dc.date.available2021-09-08T10:19:03Z-
dc.date.created2021-06-11-
dc.date.issued2010-
dc.identifier.issn1387-2877-
dc.identifier.urihttps://scholar.korea.ac.kr/handle/2021.sw.korea/118631-
dc.description.abstractCarbonic anhydrase (CA) plays a critical role in pH regulation, long-term synaptic transformation, and is associated with mental retardation, Alzheimer's disease (AD), and Down syndrome. There is accumulating evidence that CAII is increased in AD brain. The present study focused on the determination of CAII protein level in blood plasma samples using immunoblot and ELISA methods. We compared plasma from 91 AD patients (average age 74.8 y), 83 persons with amnestic mild cognitive impairment (MCI) (average age 73.7 y), and 113 cognitively normal controls (average age 70.8 y). The plasma level of CAII was significantly increased in AD patients, as compared to control groups. CAII levels were higher in males than females. There was an age-dependent increase of CAII. These results provide further evidence that changes in CAII level may play a role in the pathogenesis of AD.-
dc.languageEnglish-
dc.language.isoen-
dc.publisherIOS PRESS-
dc.subjectAUTOSOMAL RECESSIVE SYNDROME-
dc.subjectMILD COGNITIVE IMPAIRMENT-
dc.subjectRENAL TUBULAR-ACIDOSIS-
dc.subjectCEREBRAL CALCIFICATION-
dc.subjectIDENTIFICATION-
dc.subjectDIAGNOSIS-
dc.subjectOSTEOPETROSIS-
dc.subjectDEFICIENCY-
dc.subjectDEMENTIA-
dc.subjectVERSION-
dc.titlePlasma Carbonic Anhydrase II protein is Elevated in Alzheimer's Disease-
dc.typeArticle-
dc.contributor.affiliatedAuthorPark, Moon Ho-
dc.contributor.affiliatedAuthorHan, Changsu-
dc.identifier.doi10.3233/JAD-2010-100384-
dc.identifier.scopusid2-s2.0-77957272701-
dc.identifier.wosid000281903600023-
dc.identifier.bibliographicCitationJOURNAL OF ALZHEIMERS DISEASE, v.21, no.3, pp.939 - 945-
dc.relation.isPartOfJOURNAL OF ALZHEIMERS DISEASE-
dc.citation.titleJOURNAL OF ALZHEIMERS DISEASE-
dc.citation.volume21-
dc.citation.number3-
dc.citation.startPage939-
dc.citation.endPage945-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.relation.journalWebOfScienceCategoryNeurosciences-
dc.subject.keywordPlusAUTOSOMAL RECESSIVE SYNDROME-
dc.subject.keywordPlusMILD COGNITIVE IMPAIRMENT-
dc.subject.keywordPlusRENAL TUBULAR-ACIDOSIS-
dc.subject.keywordPlusCEREBRAL CALCIFICATION-
dc.subject.keywordPlusIDENTIFICATION-
dc.subject.keywordPlusDIAGNOSIS-
dc.subject.keywordPlusOSTEOPETROSIS-
dc.subject.keywordPlusDEFICIENCY-
dc.subject.keywordPlusDEMENTIA-
dc.subject.keywordPlusVERSION-
dc.subject.keywordAuthorAlzheimer&apos-
dc.subject.keywordAuthors disease-
dc.subject.keywordAuthorcarbonic anhydrase II-
dc.subject.keywordAuthormild cognitive impairment-
dc.subject.keywordAuthorplasma-
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