Polymorphisms of pro-inflammatory genes and Alzheimer's disease risk:: A pharmacogenomic approach

被引:33
作者
Candore, Giuseppina
Balistreri, Carmela Rita
Grimaldi, Maria Paola
Listi, Florinda
Vasto, Sonya
Chiappelli, Martina
Licastro, Federico
Colonna-Romano, Giuseppina
Lio, Domenico
Caruso, Calogero
机构
[1] Univ Palermo, Dipartimento Biopatol & Metodol Biomed, Grp Studio Immunosenescenza, I-90134 Palermo, Italy
[2] Univ Bologna, Dipartimento Patol Sperimentale, I-40126 Bologna, Italy
关键词
Alzheimer's disease; genetics; inflammation; pharmacogenomics;
D O I
10.1016/j.mad.2006.11.013
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Clinically and pathologically Alzheimer's disease (AD) represents a sequential progressive neurodegenerative disorder. AD is etiologically heterogeneous and accounts for a majority of dementia in western societies. Inflammation clearly occurs in pathologically vulnerable regions of the AD brain and the search for genetic factors influencing the pathogenesis of AD has lead to the identification of numerous gene polymorphisms that might act as susceptibility modifiers. Accordingly, several reports have indicated that the risk of AD is substantially influenced by several genetic polymorphisms in the promoter region, or other untranslated regions, of genes encoding inflammatory mediators, although not all the studies were replied. Here, we review several data suggesting that inflammatory genetic variation may contribute to AD susceptibility. All together this information may represent the basis both for future recognition of individuals at risk and for the pharmacogenomic driving of drug responsiveness. (c) 2006 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:67 / 75
页数:9
相关论文
共 100 条
[1]   The cyclooxygenase 2-765 C promoter allele is a protective factor for Alzheimer's disease [J].
Abdullah, L ;
Ait-Ghezala, G ;
Crawford, F ;
Crowell, TA ;
Barker, WW ;
Duara, R ;
Mullan, M .
NEUROSCIENCE LETTERS, 2006, 395 (03) :240-243
[2]   IMMUNOCHEMICAL IDENTIFICATION OF THE SERINE PROTEASE INHIBITOR ALPHA-1-ANTICHYMOTRYPSIN IN THE BRAIN AMYLOID DEPOSITS OF ALZHEIMERS-DISEASE [J].
ABRAHAM, CR ;
SELKOE, DJ ;
POTTER, H .
CELL, 1988, 52 (04) :487-501
[3]   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
[4]   Association of the toll-like receptor 4 gene Asp299Gly polymorphism with acute coronary events [J].
Ameziane, N ;
Beillat, T ;
Verpillat, P ;
Chollet-Martin, S ;
Aumont, MC ;
Seknadji, P ;
Lamotte, M ;
Lebret, D ;
Ollivier, V ;
de Prost, D .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2003, 23 (12) :E61-E64
[5]  
[Anonymous], ALZHEIMERS DIS
[6]   β-Amyloid-induced glial expression of both pro- and anti-inflammatory cytokines in cerebral cortex of aged transgenic Tg2576 mice with Alzheimer plaque pathology [J].
Apelt, J ;
Schliebs, R .
BRAIN RESEARCH, 2001, 894 (01) :21-30
[7]   TLR4 mutations are associated with endotoxin hyporesponsiveness in humans [J].
Arbour, NC ;
Lorenz, E ;
Schutte, BC ;
Zabner, J ;
Kline, JN ;
Jones, M ;
Frees, K ;
Watt, JL ;
Schwartz, DA .
NATURE GENETICS, 2000, 25 (02) :187-+
[8]  
ARONSON MK, 1991, ARCH INTERN MED, V151, P989, DOI 10.1001/archinte.1991.00400050129024
[9]   CD14 and toll-like receptor 4: a link between infection and acute coronary events? [J].
Arroyo-Espliguero, R ;
Avanzas, P ;
Jeffery, S ;
Kaski, JC .
HEART, 2004, 90 (09) :983-988
[10]  
Balasingam V, 1996, J NEUROSCI, V16, P2945