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Increased cerebrospinal fluid soluble TREM2 concentration in Alzheimer's disease.

Journal article
Authors Amanda Heslegrave
Wendy Heywood
Ross Paterson
Nadia Magdalinou
Johan Svensson
Per Johansson
Annika Öhrfelt
Kaj Blennow
John Hardy
Jonathan Schott
Kevin Mills
Henrik Zetterberg
Published in Molecular neurodegeneration
Volume 11
Issue 1
Pages 3
ISSN 1750-1326
Publication year 2016
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Institute of Medicine, Department of Internal Medicine and Clinical Nutrition
Pages 3
Language en
Links dx.doi.org/10.1186/s13024-016-0071-...
Subject categories Neurochemistry

Abstract

The discovery that heterozygous missense mutations in the gene encoding triggering receptor expressed on myeloid cells 2 (TREM2) are risk factors for Alzheimer's disease (AD), with only the apolipoprotein E (APOE) ε4 gene allele conferring a higher risk, has led to increased interest in immune biology in the brain. TREM2 is expressed on microglia, the resident immune cells of the brain and has been linked to phagocytotic clearance of amyloid β (Aβ) plaques. Soluble TREM2 (sTREM2) has previously been measured in cerebrospinal fluid (CSF) by ELISA but in our hands commercial kits have proved unreliable, suggesting that other methods may be required. We developed a mass spectrometry method using selected reaction monitoring for the presence of a TREM2 peptide, which can be used to quantify levels of sTREM2 in CSF.

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