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A polymorphism in the complement component C1r is not associated with sporadic Alzheimer's disease
Hanna Rosenmann1, Zeev Meiner, Esther Kahana
1The Agnes Ginges Center for Human Neurogenetics, Department of Neurology, Hadassah University Hospital, Ein Karem, Jerusalem 91120, Israel. rosenman@hadassah.org.il
Abstract:
A growing body of evidence suggests that Alzheimer's disease (AD) is associated with local inflammation processes. Complement activation is one of the cardinal pathological features of the inflammation. Intensive AD association studies investigating polymorphisms in inflammatory-related genes have been recently performed, mainly in cytokines, but much less has been focused on AD association with polymorphisms in complement components. We performed a case-control association study between the codon 135 polymorphism in the complement component C1r gene and sporadic AD. No association was detected with AD: neither as a risk factor, and nor as a modifier gene affecting the age at disease onset and disease progression. No interactive effect was found with apolipoprotein E e4. These findings show no evidence for association between C1r codon 135 polymorphism and AD in our population.