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Open Access Research

Monocyte chemoattractant protein-1 promoter polymorphism and plasma levels in alzheimer’s disease

Elisa Porcellini1*, Manuela Ianni1, Ilaria Carbone1, Massimo Franceschi2 and Federico Licastro1

Author Affiliations

1 DIMES, School of Medicine, University of Bologna, Via S. Giacomo 14, Bologna, 40126, Italy

2 Department of Neurology, IRCCS Multimedica, Milan, Italy

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Immunity & Ageing 2013, 10:6  doi:10.1186/1742-4933-10-6

Published: 21 February 2013

Abstract

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.

Keywords:
Alzheimer’s disease; MCP-1 promoter polymorphism; MCP-1 plasma levels; MCI –AD conversion