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dc.contributor.authorMamo, John
dc.contributor.authorJian, Le
dc.contributor.authorJames, A.
dc.contributor.authorFlicker, L.
dc.contributor.authorEsselmann, H.
dc.contributor.authorWiltfang, J.
dc.date.accessioned2017-01-30T14:38:53Z
dc.date.available2017-01-30T14:38:53Z
dc.date.created2008-11-12T23:36:30Z
dc.date.issued2008
dc.identifier.citationMamo, J. C. L. and Jian, L. and James, A. P. and Flicker, L. and Esselmann, H. and Wiltfang, J.. 2008. Plasma lipoprotein b-amyloid in subjects with Alzheimer's disease or mild cognitive impairment. Annals of Clinical Biochemistry 45 (4): 395-403.
dc.identifier.urihttp://hdl.handle.net/20.500.11937/40017
dc.identifier.doi10.1258/acb.2008.007214
dc.description.abstract

Background: Plasma amyloid -peptide (A) can compromise the blood-brain barrier, contributing to cerebrovascular alterations and amyloid angiopathy in Alzheimer's disease (AD). The objectives of this study were to investigate the distribution of lipoprotein-bound plasma-A isoforms.Methods: This involved a case-control study of subjects with AD or amnestic mild cognitive impairment (MCI) versus controls. Lipoprotein A distribution was determined in fasted plasma. For assessment of chylomicron homeostasis in the postabsorptive state, subjects were bled 4 h after a low-fat meal. The main outcome measures were plasma lipoprotein A isoform distribution and lipid homeostasis.Results: We found the majority of plasma A to be associated with triglyceride-rich lipoproteins (TRLs) encompassing chylomicrons, VLDL and IDL. For all lipoprotein groups, A1 40 was the predominant isoform, accounting for approximately 50% of the total. Thereafter, equivalent amounts of the isoforms 1 42, 2 40, 1 38, 1 37 and 1 39 were found. A1 37, A1 38 and A2 40 isoforms were significantly enriched within the TRL fraction of AD/MCI subjects and similar trends were observed for isoforms A1 39, A1 40 and A1 42. Lipoprotein-A was inversely associated with plasma total- and LDL cholesterol. AD/MCI subjects were not dyslipidaemic, however, there was evidence of accumulation of chylomicrons in the postabsorptive state.Conclusions: Our data show that A was found to be associated with plasma lipoproteins, especially those enriched with triglyceride. We find that A may be increased in normolipidaemic AD subjects, commensurate with possible disturbances in postprandial lipoprotein homeostasis.

dc.publisherRoyal Society of Medicine Press Ltd
dc.titlePlasma lipoprotein b-amyloid in subjects with Alzheimer's disease or mild cognitive impairment
dc.typeJournal Article
dcterms.source.volume45
dcterms.source.number4
dcterms.source.monthjul
dcterms.source.startPage395
dcterms.source.endPage403
dcterms.source.titleAnnals of Clinical Biochemistry
curtin.note

Copyright 2008 Blackwell Publishin.

curtin.note

Please refer to the publisher for the definitive published version.

curtin.identifierEPR-2954
curtin.accessStatusOpen access via publisher
curtin.facultySchool of Public Health
curtin.facultyDivision of Health Sciences


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