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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.

Original publication

DOI

10.1007/s12017-007-8013-y

Type

Journal article

Journal

Neuromolecular Med

Publication Date

2007

Volume

9

Pages

331 - 334

Keywords

Age of Onset, Aged, Alzheimer Disease, Amino Acid Substitution, Cohort Studies, Complement Factor H, DNA, Gene Frequency, Genetic Predisposition to Disease, Genotype, Humans, Polymorphism, Single Nucleotide