Association between the polymorphism of CCR5 and Alzheimer's disease - Results of a study performed on male and female patients from Northern Italy

被引:23
作者
Balistreri, Carmela Rita
Grimaldi, Maria Paola
Vasto, Sonya
Listi, Florinda
Chiappelli, Martina
Licastro, Federico
Lio, Domenico
Caruso, Calogero
Candore, Giuseppina
机构
[1] Univ Palermo, Grp Studio Immunosenescenza, Dipartimento Biopatol & Metodol Biomed, I-90134 Palermo, Italy
[2] Univ Bologna, Dipartimento Patol Sperimentale, Bologna, Italy
来源
ESTROGENS AND HUMAN DISEASES | 2006年 / 1089卷
关键词
Alzheimer's disease; CCR5; immunogenetics; inflammation; women;
D O I
10.1196/annals.1386.012
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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 beta-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 Delta 32 (a 32-by 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 CCR Delta 32 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.
引用
收藏
页码:454 / 461
页数:8
相关论文
共 42 条
[1]   Inflammation and Alzheimer's disease [J].
Akiyama, H ;
Barger, S ;
Barnum, S ;
Bradt, B ;
Bauer, J ;
Cole, GM ;
Cooper, NR ;
Eikelenboom, P ;
Emmerling, M ;
Fiebich, BL ;
Finch, CE ;
Frautschy, S ;
Griffin, WST ;
Hampel, H ;
Hull, M ;
Landreth, G ;
Lue, LF ;
Mrak, R ;
Mackenzie, IR ;
McGeer, PL ;
O'Banion, MK ;
Pachter, J ;
Pasinetti, G ;
Plata-Salaman, C ;
Rogers, J ;
Rydel, R ;
Shen, Y ;
Streit, W ;
Strohmeyer, R ;
Tooyoma, I ;
Van Muiswinkel, FL ;
Veerhuis, R ;
Walker, D ;
Webster, S ;
Wegrzyniak, B ;
Wenk, G ;
Wyss-Coray, T .
NEUROBIOLOGY OF AGING, 2000, 21 (03) :383-421
[2]   Neuroprotective effects of female gonadal steroids in reproductively senescent female rats [J].
Alkayed, NJ ;
Murphy, SJ ;
Traystman, RJ ;
Hurn, PD .
STROKE, 2000, 31 (01) :161-167
[3]  
[Anonymous], 1987, DIAGNOSTIC STAT MANU, V4th
[4]   Characterization of chemokines and their receptors in the central nervous system: physiopathological implications [J].
Bajetto, A ;
Bonavia, R ;
Barbero, S ;
Schettini, G .
JOURNAL OF NEUROCHEMISTRY, 2002, 82 (06) :1311-1329
[5]   CXC and CC chemokine receptors on coronary and brain endothelia [J].
Berger, O ;
Gan, XH ;
Gujuluva, C ;
Burns, AR ;
Sulur, G ;
Stins, M ;
Way, D ;
Witte, M ;
Weinand, M ;
Said, J ;
Kim, KS ;
Taub, D ;
Graves, MC ;
Fiala, M .
MOLECULAR MEDICINE, 1999, 5 (12) :795-805
[6]   Opposite Role of Pro-Inflammatory Alleles in Acute Myocardial Infarction and Longevity Results of Studies Performed in a Sicilian Population [J].
Candore, Giuseppina ;
Balistreri, Carmela Rita ;
Grimaldi, Maria Paola ;
Listi, Florinda ;
Vasto, Sonya ;
Caruso, Marco ;
Caimi, Gregorio ;
Hoffmann, Enrico ;
Colonna-Romano, Giuseppina ;
Lio, Domenico ;
Paolisso, Giuseppe ;
Franceschi, Claudio ;
Caruso, Calogero .
UNDERSTANDING AND MODULATING AGING, 2006, 1067 :270-275
[7]  
Caruso C, 2003, NEW ENGL J MED, V349, P193
[8]   The chemokine receptor CCR5-Δ32 gene mutation is not protective against Alzheimer's disease [J].
Combarros, O ;
Infante, J ;
Llorca, J ;
Peña, N ;
Fernández-Viadero, C ;
Berciano, J .
NEUROSCIENCE LETTERS, 2004, 366 (03) :312-314
[9]   A method for estimating progression rates in Alzheimer disease [J].
Doody, RS ;
Massman, P ;
Dunn, JK .
ARCHIVES OF NEUROLOGY, 2001, 58 (03) :449-454
[10]   Neuroinflammation in Alzheimer's disease and prion disease [J].
Eikelenboom, P ;
Bate, C ;
Van Gool, WA ;
Hoozemans, JJM ;
Rozemuller, JM ;
Veerhuis, R ;
Williams, A .
GLIA, 2002, 40 (02) :232-239