Lack Of Association Between Theccr5-Delta32 Polymorphism And Neurodegenerative Disorders

Objective: Recent studies have suggested that diminished Ccr5 functioning has an effect on synaptic plasticity and hippocampal memory in mouse models.CCR5-delta32, a 32-bp frameshift deletion in humanCCR5encoding a nonfunctional receptor, has been reported to have a protective effect against human immunodeficiency virus infection but its role as a modifier of neurodegenerative disease has been minimally explored. We investigated whether theCCR5-delta32 polymorphism could have an effect in the context of human neurodegenerative diseases. Methods: We examined the frequency of theCCR5-delta32 polymorphism in a large and well-characterized cohort including 1425 patients with neurodegenerative dementias and 2032 controls. Results: We did not observe a significant association between theCCR5-delta32 polymorphism and any of the neurodegenerative diseases screened in this study. However, we observed an earlier age of onset among neurodegenerative disease patients carrying theCCR5-delta32 allele. Conclusions: Although our findings were inconclusive, the earlier age of onset observed among neurodegenerative disease patients carrying theCCR5-delta32 allele suggests that the deletion may have a detrimental effect in the context of neurodegeneration.