Complement factor H Y402H polymorphism is not associated with late-onset Alzheimer's disease.
There is evidence to suggest a role for immune dysfunction in the pathogenesis of Alzheimer's disease, and it has previously been shown that blood plasma levels of the protein complement factor H, a member of the alternative complement pathway, was specifically elevated in people with late-onset Alzheimer's disease. We have genotyped the common complement factor H Y402H polymorphism in a large case-control cohort to investigate association with late-onset Alzheimer's disease susceptibility and find no evidence that this SNP is associated with disease risk. However, it remains possible that another variant in this gene may modify susceptibility for late-onset Alzheimer's disease.
Hamilton
Gillian
G
MRC Centre for Neurodegeneration, Institute for Psychiatry, Kings College London, Denmark Hill, London SE5 8AF, UK. G.Hamilton@iop.kcl.ac.uk
Proitsi
Petra
P
Williams
Julie
J
O'Donovan
Michael
M
Owen
Michael
M
Powell
John
J
Lovestone
Simon
S
D017668:Age of Onset; D000368:Aged; D000544:Alzheimer Disease / Q000235:genetics*; D019943:Amino Acid Substitution; D015331:Cohort Studies; D017242:Complement Factor H / Q000235:genetics*; D004247:DNA / Q000097:blood / Q000235:genetics / Q000302:isolation & purification; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D020641:Polymorphism, Single Nucleotide
D017242:Complement Factor H; D004247:DNA