Systemic complement activation in age-related macular degeneration

Dysregulation of the alternative pathway (AP) of complement cascade has been implicated in the pathogenesis of age-related macular degeneration (AMD), the leading cause of blindness in the elderly. To further test the hypothesis that defective control of complement activation underlies AMD, paramete...

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Bibliographic Details
Published in:PloS one 2008-07, Vol.3 (7), p.e2593-e2593
Main Authors: Scholl, Hendrik P N, Charbel Issa, Peter, Walier, Maja, Janzer, Stefanie, Pollok-Kopp, Beatrix, Börncke, Florian, Fritsche, Lars G, Chong, Ngaihang V, Fimmers, Rolf, Wienker, Thomas, Holz, Frank G, Weber, Bernhard H F, Oppermann, Martin
Format: Article
Language:English
Subjects:
Age
Age related diseases
Aged
Aged, 80 and over
Alternative pathway
Anticoagulants
Biometrics
Blindness
Blood plasma
Case-Control Studies
Complement
Complement Activation
Complement component C2
Complement component C3
Complement component C3d
Complement component C4
Complement component C5a
Complement factor B
Complement factor H
Complement Factor H - genetics
Complement Factor H - metabolism
Correlation analysis
Digitization
Enzymes
Epidemiology
Female
Genes
Genetic aspects
Genetic diversity
Genetic markers
Genetic variance
Genetic Variation
Genetics and Genomics/Genetics of Disease
Genotype
Geriatrics
Haplotypes
Humans
Immunoassay
Immunology
Immunology/Innate Immunity
Informatics
Macular degeneration
Macular Degeneration - genetics
Macular Degeneration - immunology
Male
Markers
Older people
Ophthalmology/Inherited Eye Disorders
Ophthalmology/Macular Disorders
Pathogenesis
Patients
Physiological aspects
Plasma
Polymorphism, Single Nucleotide
Population studies
Proteins
Regression analysis
Regulators
Risk Factors
Single nucleotide polymorphisms
Single-nucleotide polymorphism
Studies
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Summary:Dysregulation of the alternative pathway (AP) of complement cascade has been implicated in the pathogenesis of age-related macular degeneration (AMD), the leading cause of blindness in the elderly. To further test the hypothesis that defective control of complement activation underlies AMD, parameters of complement activation in blood plasma were determined together with disease-associated genetic markers in AMD patients. Plasma concentrations of activation products C3d, Ba, C3a, C5a, SC5b-9, substrate proteins C3, C4, factor B and regulators factor H and factor D were quantified in patients (n = 112) and controls (n = 67). Subjects were analyzed for single nucleotide polymorphisms in factor H (CFH), factor B-C2 (BF-C2) and complement C3 (C3) genes which were previously found to be associated with AMD. All activation products, especially markers of chronic complement activation Ba and C3d (p
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0002593