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Plasma amyloid-β in patients with Tangier disease.

Journal article
Authors Pashtun Shahim
Andrea E Bochem
Niklas Mattsson
Ronald Lautner
Kaj Blennow
G Kees Hovingh
M Mahdi Motazacker
Henrik Zetterberg
Published in Journal of Alzheimer's disease : JAD
Volume 35
Issue 2
Pages 307-12
ISSN 1875-8908
Publication year 2013
Published at
Pages 307-12
Language en
Subject categories Neurosciences, Neurochemistry

Abstract

Tangier disease (TD) is a rare genetic disorder caused by mutations in the ATP-binding cassette transporter A1 (ABCA1) gene, which results in impaired cellular cholesterol efflux and high-density lipoprotein cholesterol deficiency. Animal and in vitro studies indicate that ABCA1 is involved in the production of amyloid-β (Aβ), a pivotal protein in Alzheimer's disease. We here examined whether plasma Aβ levels are altered in TD patients. Plasma from 5 TD patients and 5 controls were analyzed for Aβ1-40, Aβ1-42, AβX-40, and AβX-42 but no differences were found. In conclusion, loss of ABCA1 function may not have any profound effect on Aβ metabolism in humans, at least not in the periphery, as reflected by plasma Aβ levels.

Page Manager: Webmaster|Last update: 9/11/2012
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