PMID- 24022074
OWN - NLM
STAT- MEDLINE
DCOM- 20141216
LR  - 20140429
IS  - 1660-2862 (Electronic)
IS  - 1660-2854 (Linking)
VI  - 13
IP  - 4
DP  - 2014
TI  - Effect of proinflammatory gene polymorphisms on the risk of Alzheimer's disease.
PG  - 230-6
LID - 10.1159/000353395 [doi]
AB  - BACKGROUND: A number of studies associate Alzheimer's disease (AD) with APOE 
      polymorphism and alleles which favor the increased expression of immunological 
      mediators such as cytokines or acute-phase proteins. OBJECTIVE: In this study we 
      evaluated the distribution of a set of functionally important polymorphisms of 
      genes encoding prototypical inflammatory molecules in individuals with AD. We 
      also investigated whether a synergistic effect of these proinflammatory gene 
      polymorphisms on the risk of AD could be hypothesized. METHODS: In a genetic 
      association study that included 533 AD patients and 713 controls, the following 
      gene polymorphisms were analyzed: C-reactive protein (CRP) 1059 G/C, interleukin 
      6 (IL6) -174 G/C, interleukin 1beta (IL1B) -31 T/C, tumor necrosis factor alpha (TNF-alpha) 
      -308 G/A, macrophage migration inhibitory factor (MIF) -173 G/C, monocyte 
      chemoattractant protein 1 (CCL2) -2518 A/G, intercellular adhesion molecule 1 
      (ICAM1) 469 E/K, E-selectin (SELE) Ser128Arg, macrophage inflammatory protein 1alpha 
      (CCL3) -906 T/A, matrix metalloproteinase 3 (MMP3) -1171 5A/6A and matrix 
      metalloproteinase 9 (MMP9) -1562 C/T. RESULTS: We found that IL6, IL1B, CCL2, 
      CCL3, SELE, ICAM1, MMP3, and MMP9 gene polymorphisms were significantly and 
      independently associated with AD. The association remained significant even after 
      the Bonferroni correction. We also found that these proinflammatory polymorphisms 
      were associated with different levels of risk for AD, depending on the number of 
      high-risk genotypes concomitantly carried by a given individual. CONCLUSION: 
      Proinflammatory genotypes might influence the development and progression of AD 
      exerting a potential synergistic effect.
CI  - Copyright (c) 2013 S. Karger AG, Basel.
FAU - Flex, Andrea
AU  - Flex A
AD  - Department of Medicine, A. Gemelli University Hospital, Catholic University 
      School of Medicine, Rome, Italy.
FAU - Giovannini, Silvia
AU  - Giovannini S
FAU - Biscetti, Federico
AU  - Biscetti F
FAU - Liperoti, Rosa
AU  - Liperoti R
FAU - Spalletta, Gianfranco
AU  - Spalletta G
FAU - Straface, Giuseppe
AU  - Straface G
FAU - Landi, Francesco
AU  - Landi F
FAU - Angelini, Flavia
AU  - Angelini F
FAU - Caltagirone, Carlo
AU  - Caltagirone C
FAU - Ghirlanda, Giovanni
AU  - Ghirlanda G
FAU - Bernabei, Roberto
AU  - Bernabei R
LA  - eng
PT  - Journal Article
DEP - 20130906
PL  - Switzerland
TA  - Neurodegener Dis
JT  - Neuro-degenerative diseases
JID - 101189034
RN  - 0 (Antigens, CD)
RN  - 0 (Cytokines)
RN  - 9007-41-4 (C-Reactive Protein)
RN  - EC 3.4.24.7 (Matrix Metalloproteinase 1)
SB  - IM
MH  - Aged
MH  - Alzheimer Disease/diagnosis/*genetics
MH  - Antigens, CD/genetics
MH  - C-Reactive Protein/genetics
MH  - Cytokines/genetics
MH  - Female
MH  - Genetic Association Studies
MH  - Humans
MH  - Inflammation/genetics
MH  - Male
MH  - Matrix Metalloproteinase 1/genetics
MH  - *Polymorphism, Genetic
MH  - Risk Factors
EDAT- 2013/09/12 06:00
MHDA- 2014/12/17 06:00
CRDT- 2013/09/12 06:00
PHST- 2013/01/10 00:00 [received]
PHST- 2013/05/30 00:00 [accepted]
PHST- 2013/09/12 06:00 [entrez]
PHST- 2013/09/12 06:00 [pubmed]
PHST- 2014/12/17 06:00 [medline]
AID - 000353395 [pii]
AID - 10.1159/000353395 [doi]
PST - ppublish
SO  - Neurodegener Dis. 2014;13(4):230-6. doi: 10.1159/000353395. Epub 2013 Sep 6.