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Soluble TREM-2 in cerebrospinal fluid from patients with multiple sclerosis treated with natalizumab or mitoxantrone.

Journal article
Authors Annika Öhrfelt
Markus Axelsson
Clas Malmeström
Lenka Novakova
Amanda Heslegrave
Kaj Blennow
Jan Lycke
Henrik Zetterberg
Published in Multiple sclerosis (Houndmills, Basingstoke, England)
Volume 22
Issue 12
Pages 1587-1595
ISSN 1477-0970
Publication year 2016
Published at Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Institute of Neuroscience and Physiology, Department of Clinical Neuroscience
Pages 1587-1595
Language en
Links dx.doi.org/10.1177/1352458515624558
Subject categories Neurochemistry

Abstract

Microglia-mediated proteolysis of the triggering receptor expressed on myeloid cells-2 (TREM-2) produces soluble TREM-2 (sTREM-2) that can be measured in cerebrospinal fluid (CSF) samples. Loss-of-function mutations in TREM2 or in the gene encoding its adaptor protein cause the rare Nasu-Hakola disease (NHD). Multiple sclerosis (MS) is an autoimmune disease that in common with NHD is characterized by demyelination and microglial activation.

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Denna text är utskriven från följande webbsida:
http://www.gu.se/english/research/publication/?publicationId=231694
Utskriftsdatum: 2019-10-20