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Association between the Polymorphism of CCR5 and Alzheimer's Disease
Author(s) -
BALISTRERI CARMELA RITA,
GRIMALDI MARIA PAOLA,
VASTO SONYA,
LISTI FLORINDA,
CHIAPPELLI MARTINA,
LICASTRO FEDERICO,
LIO DOMENICO,
CARUSO CALOGERO,
CANDORE GIUSEPPINA
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1386.012
Subject(s) - association (psychology) , alzheimer's disease , polymorphism (computer science) , disease , medicine , genetics , genotype , biology , psychology , gene , psychotherapist
Alzheimer's disease (AD) is the most common cause of dementia in Western society. The prevalence of AD is greater in women than in men, largely due to longevity and survival differences favoring women. However, some studies suggest that incidence rates may really be increased in women. One possible factor influencing AD incidence in women is the loss of ovarian estrogens production after menopause, which might be involved in AD pathogenesis. Estrogens seem to influence some neuronal functions. Many of these actions appear beneficial (i.e., neuroprotective action against a variety of insults, as oxidative stress, and reduction of β‐amyloid plaques formation). Furthermore, several studies have shown that proinflammatory genotypes seem to significantly contribute to AD risk. In the present study, we evaluated whether the anti‐inflammatory allele of chemokine receptor CCR5 is a component of the genetic protective background versus AD neuronal degeneration. We genotyped for Δ32 (a 32‐bp deletion of the CCR5 gene that causes a frameshift at amino acid 185) in 191 AD patients (133 women and 58 men; age range: 53–98 years; mean age: 74.88 ± 8.44) and 182 controls (98 women and 84 men; age range: 65–93; mean age 73.21 ± 8.24) from northern Italy. No different distribution of the CCRΔ32 deletion in the two cohorts was clearly evident. Statistical analysis by gender stratification, demonstrated no differences in genotype distribution and allelic frequency both in women and in men. Further, studies should focus on identification of proinflammatory genetic variants involved in AD pathogenesis in women.