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Reduced cerebrospinal fluid BACE1 activity in multiple sclerosis.

Journal article
Authors Niklas Mattsson
M Axelsson
Sara Haghighi
Clas Malmeström
G Wu
Rolf Anckarsäter
S Sankaranarayanan
Ulf Andreasson
S Fredrikson
A Gundersen
L Johnsen
T Fladby
Andrej Tarkowski
E Trysberg
Anders Wallin
Henrik Anckarsäter
Jan Lycke
Oluf Andersen
A J Simon
Kaj Blennow
Henrik Zetterberg
Published in Multiple sclerosis (Houndmills, Basingstoke, England)
Volume 15
Issue 4
Pages 448-54
ISSN 1352-4585
Publication year 2009
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 Medicine, Department of Rheumatology and Inflammation Research
Pages 448-54
Language en
Links dx.doi.org/10.1177/1352458508100031
Keywords Adult, Aged, Amyloid Precursor Protein Secretases, cerebrospinal fluid, Amyloid beta-Protein, cerebrospinal fluid, Amyloid beta-Protein Precursor, cerebrospinal fluid, Aspartic Acid Endopeptidases, cerebrospinal fluid, Female, Humans, Lupus Erythematosus, Systemic, metabolism, Male, Middle Aged, Multiple Sclerosis, metabolism, Myelin Sheath, metabolism, Nerve Regeneration, physiology, Peptide Fragments, cerebrospinal fluid, Young Adult
Subject categories Neurochemistry, Chemistry

Abstract

BACKGROUND: Cell and animal experiments have shown that beta-site APP-cleaving enzyme 1 (BACE1) may be involved in myelination. OBJECTIVE: Here, we assess the association of cerebrospinal fluid (CSF) BACE1 activity with multiple sclerosis (MS). METHODS: BACE1 activity and levels of secreted amyloid precursor protein (APP) and amyloid-beta (Abeta) isoforms were analyzed in CSF from 100 patients with MS and 114 neurologically healthy controls. Patients with systemic lupus erythematosus (SLE), 26 with and 41 without cerebral engagement, were also included to enable comparisons with regards to another autoimmune disease. A subset of patients with MS and controls underwent a second lumbar puncture after 10 years. RESULTS: MS patients had lower CSF BACE1 activity than controls (P = 0.03) and patients with cerebral SLE (P < 0.001). Patients with cerebral SLE had higher BACE1 activity than any other group (P < 0.05 for all comparisons). BACE1 activity correlated with the different amyloid markers in all study groups. BACE1 activity decreased over 10 years in the MS group (P = 0.039) and correlated weakly with clinical disease severity scores in an inverse manner. CONCLUSIONS: These results suggest an involvement of BACE1 in the MS disease process.

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