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Cerebrospinal fluid levels of complement proteins C3, C4 and CR1 in Alzheimer's disease.

Journal article
Authors Jonny Daborg
Ulf Andreasson
Marcela Pekna
Ronald Lautner
Eric Hanse
Lennart Minthon
Kaj Blennow
Oskar Hansson
Henrik Zetterberg
Published in Journal of neural transmission (Vienna, Austria : 1996)
Volume 119
Issue 7
Pages 789-97
ISSN 1435-1463
Publication year 2012
Published at Institute of Neuroscience and Physiology, Department of Physiology
Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Pages 789-97
Language en
Keywords Adult, Aged, Aged, 80 and over, Alzheimer Disease, cerebrospinal fluid, Amyloid beta-Peptides, cerebrospinal fluid, Complement C3, cerebrospinal fluid, Complement C4, cerebrospinal fluid, Disease Progression, Female, Humans, Male, Middle Aged, Mild Cognitive Impairment, cerebrospinal fluid, Peptide Fragments, cerebrospinal fluid, Receptors, Complement, metabolism, tau Proteins, cerebrospinal fluid
Subject categories Clinical Medicine


Alzheimer's disease (AD) is strongly associated with loss of synapses. The complement system has been shown to be involved in synaptic elimination. Several studies point to an association between AD and the complement system. The purpose of this study was to examine the association of cerebrospinal fluid (CSF) levels of complement components 3 and 4 (C3 and C4, respectively), and complement receptor 1 (CR1) with AD in 43 patients with AD plus dementia, 42 patients with mild cognitive impairment (MCI) who progressed to AD during follow-up (MCI-AD), 42 patients with stable MCI and 44 controls. Complement levels were also applied in a multivariate model to determine if they provided any added value to the core AD biomarkers Aβ42, T-tau and P-tau. We found elevated CSF levels of C3 and C4 in AD compared with MCI without progression to AD, and elevated CSF levels of CR1 in MCI-AD and AD when these groups were merged. These results provide support for aberrant complement regulation as a part in the AD process, but the changes are not diagnostically useful.

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