PMID- 23432970
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20130401
LR  - 20211021
IS  - 1742-4933 (Print)
IS  - 1742-4933 (Electronic)
IS  - 1742-4933 (Linking)
VI  - 10
IP  - 1
DP  - 2013 Feb 21
TI  - Monocyte chemoattractant protein-1 promoter polymorphism and plasma levels in 
      alzheimer's disease.
PG  - 6
LID - 10.1186/1742-4933-10-6 [doi]
AB  - BACKGROUND: Neurodegenerative disorders such Alzheimer's disease (AD) are often 
      characterized by senile plaques and neurofibrillary tangle. In addition, reactive 
      astrogliosis, microglia activation and a chronic inflammation are found in AD 
      brain. Activated microglia has been reported to express a large number of beta 
      chemokines including monocyte chemoattractant protein-1 (MCP-1). The potential 
      role of MCP-1 in AD pathogenesis is supported by the over expression of MCP-1 
      associated with an increase of amyloid deposition in transgenic mice. MCP-1 
      protein may be regulated by a single nucleotide polymorphism (SNP) occurring at 
      position -2518 of the MCP-1 gene promoter. In this paper we correlated the 
      A-2518G MCP-1 SNP distribution in three different populations: AD, control and 
      MCI (mild cognitive impairment) population to evaluate whether this SNP might be 
      a risk factor for AD or for MCI-AD conversion. MCP-1 plasma levels were also 
      measured and correlated to the cognitive impairment (CIND) and AD risk. RESULTS: 
      No differences in genotype distribution and allele frequencies of A-2518G MCP-1 
      SNP among AD patients, MCI subjects and controls were observed even after APOEe4 
      variation adjustment with logistic regression. However in MCI subjects, followed 
      up for two years, this SNP appears to influence the progression of the disease; 
      being the G allele slightly more frequent in MCI patients that developed AD. 
      MCP-1 plasma levels were different among CIND (cognitive impairment but no 
      dementia), AD and controls. The MCP-1 A-2518G promoter polymorphism did not 
      affect MCP-1 plasma levels within the three populations. CONCLUSIONS: MCP-1 G 
      allele did not affect the risk of AD, but slightly influenced MCI conversion to 
      AD and MCP-1 plasma levels were increased in subjects with preclinical AD.
FAU - Porcellini, Elisa
AU  - Porcellini E
AD  - DIMES, School of Medicine, University of Bologna, Via S, Giacomo 14, Bologna, 
      40126, Italy. elisa.porcellini3@unibo.it.
FAU - Ianni, Manuela
AU  - Ianni M
FAU - Carbone, Ilaria
AU  - Carbone I
FAU - Franceschi, Massimo
AU  - Franceschi M
FAU - Licastro, Federico
AU  - Licastro F
LA  - eng
PT  - Journal Article
DEP - 20130221
PL  - England
TA  - Immun Ageing
JT  - Immunity & ageing : I & A
JID - 101235427
PMC - PMC3610278
EDAT- 2013/02/26 06:00
MHDA- 2013/02/26 06:01
PMCR- 2013/02/21
CRDT- 2013/02/26 06:00
PHST- 2012/11/29 00:00 [received]
PHST- 2013/02/16 00:00 [accepted]
PHST- 2013/02/26 06:00 [entrez]
PHST- 2013/02/26 06:00 [pubmed]
PHST- 2013/02/26 06:01 [medline]
PHST- 2013/02/21 00:00 [pmc-release]
AID - 1742-4933-10-6 [pii]
AID - 10.1186/1742-4933-10-6 [doi]
PST - epublish
SO  - Immun Ageing. 2013 Feb 21;10(1):6. doi: 10.1186/1742-4933-10-6.