Complement Protein Isoforms in CSF as Possible Biomarkers for Neurodegenerative Disease

It has been suggested that the activation of the complement system is involved in the pathogenesis of several neurodegenerative diseases including Alzheimer’s disease (AD), Parkinson’s disease (PD), and multiple sclerosis (MS). Here, the CSF expression levels of complement proteins C3b, C4b, factor...

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Main Authors: Finehout, Erin J., Franck, Zsofia, Lee, Kelvin H.
Format: Online
Language:English
Published: IOS Press 2005
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3851089/
id pubmed-3851089
recordtype oai_dc
spelling pubmed-38510892013-12-22 Complement Protein Isoforms in CSF as Possible Biomarkers for Neurodegenerative Disease Finehout, Erin J. Franck, Zsofia Lee, Kelvin H. Other It has been suggested that the activation of the complement system is involved in the pathogenesis of several neurodegenerative diseases including Alzheimer’s disease (AD), Parkinson’s disease (PD), and multiple sclerosis (MS). Here, the CSF expression levels of complement proteins C3b, C4b, factor B, and factor H were compared between normal subjects and patients diagnosed with AD, PD, MS, and neurosyphilis. The CSF proteins were initially separated using two-dimensional gel electrophoresis, which allowed the comparison of some of the individual complement isoforms. Patients with AD, PD, and MS all showed more than one complement isoform with a significant change (p < 0.05) in CSF expression level compared to normal subjects. PD patients were found to have the greatest number of significantly changed isoforms, all showing a decreased expression level in PD CSF. The complement isoforms examined were able to distinguish between some, but not all, of the diseases studied. The data suggest that when investigating a protein as a possible biomarker, it may be useful to compare individual protein isoform expression levels in addition to the more commonly measured total protein expression level. IOS Press 2005 2005-05-26 /pmc/articles/PMC3851089/ /pubmed/15920296 http://dx.doi.org/10.1155/2005/806573 Text en Copyright © 2005 Hindawi Publishing Corporation.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Finehout, Erin J.
Franck, Zsofia
Lee, Kelvin H.
spellingShingle Finehout, Erin J.
Franck, Zsofia
Lee, Kelvin H.
Complement Protein Isoforms in CSF as Possible Biomarkers for Neurodegenerative Disease
author_facet Finehout, Erin J.
Franck, Zsofia
Lee, Kelvin H.
author_sort Finehout, Erin J.
title Complement Protein Isoforms in CSF as Possible Biomarkers for Neurodegenerative Disease
title_short Complement Protein Isoforms in CSF as Possible Biomarkers for Neurodegenerative Disease
title_full Complement Protein Isoforms in CSF as Possible Biomarkers for Neurodegenerative Disease
title_fullStr Complement Protein Isoforms in CSF as Possible Biomarkers for Neurodegenerative Disease
title_full_unstemmed Complement Protein Isoforms in CSF as Possible Biomarkers for Neurodegenerative Disease
title_sort complement protein isoforms in csf as possible biomarkers for neurodegenerative disease
description It has been suggested that the activation of the complement system is involved in the pathogenesis of several neurodegenerative diseases including Alzheimer’s disease (AD), Parkinson’s disease (PD), and multiple sclerosis (MS). Here, the CSF expression levels of complement proteins C3b, C4b, factor B, and factor H were compared between normal subjects and patients diagnosed with AD, PD, MS, and neurosyphilis. The CSF proteins were initially separated using two-dimensional gel electrophoresis, which allowed the comparison of some of the individual complement isoforms. Patients with AD, PD, and MS all showed more than one complement isoform with a significant change (p < 0.05) in CSF expression level compared to normal subjects. PD patients were found to have the greatest number of significantly changed isoforms, all showing a decreased expression level in PD CSF. The complement isoforms examined were able to distinguish between some, but not all, of the diseases studied. The data suggest that when investigating a protein as a possible biomarker, it may be useful to compare individual protein isoform expression levels in addition to the more commonly measured total protein expression level.
publisher IOS Press
publishDate 2005
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3851089/
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