Plasma lipoprotein β-amyloid in subjects with Alzheimer’s disease or mild cognitive impairment

Ann Clin Biochem 2008;45:395-403
doi:10.1258/acb.2008.007214
© 2008 Association for Clinical Biochemistry

 

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Original Articles


J C L Mamo1,
L Jian1,
A P James1,
L Flicker2,
H Esselmann3 and
J Wiltfang3


1 Division of Health Sciences, Curtin University of Technology and ATN Centre for Metabolic Health and Fitness;
2 School of Medicine and Pharmacology Royal Perth Hospital Unit, University of Western Australia, Perth, Western Australia 6009, Australia;
3 Laboratory of Molecular Neurobiology, Department of Psychiatry, University of Erlangen-Nuremberg, Erlangen 91054, Germany


Corresponding author: Prof John Mamo. Email: J.Mamo{at}Curtin.edu.au


Background: Plasma amyloid β-peptide (Aβ) can compromise the blood-brainbarrier, contributing to cerebrovascular alterations and amyloidangiopathy in Alzheimer’s disease (AD). The objectives of thisstudy were to investigate the distribution of lipoprotein-boundplasma-Aβ isoforms.

Methods: This involved a case-control study of subjects with AD or amnesticmild cognitive impairment (MCI) versus controls. LipoproteinAβ distribution was determined in fasted plasma. For assessmentof chylomicron homeostasis in the postabsorptive state, subjectswere bled 4 h after a low-fat meal. The main outcome measureswere plasma lipoprotein Aβ isoform distribution and lipidhomeostasis.

Results: We found the majority of plasma Aβ to be associated with triglyceride-rich lipoproteins (TRLs) encompassing chylomicrons, VLDL and IDL. For all lipoprotein groups, Aβ1–40 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. Aβ1–37, Aβ1–38 and Aβ2–40 isoforms were significantly enriched within the TRL fraction of AD/MCI subjects and similar trends were observed for isoforms Aβ1–39, Aβ1–40 and Aβ1–42.Lipoprotein-Aβ was inversely associated with plasma total-and LDL cholesterol. AD/MCI subjects were not dyslipidaemic,however, there was evidence of accumulation of chylomicronsin the postabsorptive state.

Conclusions: Our data show that Aβ was found to be associated with plasmalipoproteins, especially those enriched with triglyceride. Wefind that Aβ may be increased in normolipidaemic AD subjects,commensurate with possible disturbances in postprandial lipoproteinhomeostasis.

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