Annals of Clinical Biochemistry > Volume 45, Number 4 > Pp. 395-403

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Original Articles

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

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-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-Aβ isoforms.

Methods: This involved a case-control study of subjects with AD or amnestic mild cognitive impairment (MCI) versus controls. Lipoprotein Aβ 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 Aβ isoform distribution and lipid homeostasis.

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, Aβ_1–40 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. Aβ_1–37, Aβ_1–38 and Aβ_2–40 isoforms were significantly enriched within the TRL fraction of AD/MCI subjects and similar trends were observed for isoforms Aβ_1–39, Aβ_1–40 and Aβ_1–42. Lipoprotein-Aβ was inversely associated with plasma total- and LDL cholesterol. AD/MCI subjects were not dyslipidaemic, however, there was evidence of accumulation of chylomicrons in the postabsorptive state.

Conclusions: Our data show that Aβ was found to be associated with plasma lipoproteins, especially those enriched with triglyceride. We find that Aβ may be increased in normolipidaemic AD subjects, commensurate with possible disturbances in postprandial lipoprotein homeostasis.

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