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Plasma MCP-1 and Cognitive Decline in Patients with Alzheimer’s Disease and Mild Cognitive Impairment: A Two-year Follow-up Study

Monocyte chemoattractant protein-1 (MCP-1, also known as chemokine CCL2) is a vital chemokine that mediates inflammation in Alzheimer’s disease (AD). We analyzed the associations between the baseline plasma MCP-1 level, longitudinal cognitive changes, and genetic effects of CCL2 rs1024611 and its re...

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Autores principales: Lee, Wei-Ju, Liao, Yi-Chu, Wang, Yen-Feng, Lin, I-Feng, Wang, Shuu-Jiun, Fuh, Jong-Ling
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5775300/
https://www.ncbi.nlm.nih.gov/pubmed/29352259
http://dx.doi.org/10.1038/s41598-018-19807-y
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author Lee, Wei-Ju
Liao, Yi-Chu
Wang, Yen-Feng
Lin, I-Feng
Wang, Shuu-Jiun
Fuh, Jong-Ling
author_facet Lee, Wei-Ju
Liao, Yi-Chu
Wang, Yen-Feng
Lin, I-Feng
Wang, Shuu-Jiun
Fuh, Jong-Ling
author_sort Lee, Wei-Ju
collection PubMed
description Monocyte chemoattractant protein-1 (MCP-1, also known as chemokine CCL2) is a vital chemokine that mediates inflammation in Alzheimer’s disease (AD). We analyzed the associations between the baseline plasma MCP-1 level, longitudinal cognitive changes, and genetic effects of CCL2 rs1024611 and its receptor, CC-chemokine receptor 2 (CCR2) rs1799864, in AD. In total, 310 AD patients and 66 mild cognitive impairment (MCI) patients were followed for 2 years, and 120 controls were recruited at baseline for comparison. After adjusting for covariates using one-way analysis of covariance, AD patients had higher plasma MCP-1 levels compared with MCI patients and controls, and severe AD patients had the highest levels. After adjusting for covariates using generalized estimating equation analysis, the results showed that the baseline MCP-1 level was significantly correlated with changes in the two-year Mini-Mental Status Examination (p = 0.046). The A allele of CCR2 rs1799864 was associated with a higher MCP-1 level in AD and MCI patients. In conclusion, plasma MCP-1 might reflect the risk and disease course of AD. A higher plasma MCP-1 level is associated with greater severity and faster cognitive decline. Additionally, the CCR2 polymorphism may play a role in the regulation of MCP-1/CCR2 signaling in AD.
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spelling pubmed-57753002018-01-26 Plasma MCP-1 and Cognitive Decline in Patients with Alzheimer’s Disease and Mild Cognitive Impairment: A Two-year Follow-up Study Lee, Wei-Ju Liao, Yi-Chu Wang, Yen-Feng Lin, I-Feng Wang, Shuu-Jiun Fuh, Jong-Ling Sci Rep Article Monocyte chemoattractant protein-1 (MCP-1, also known as chemokine CCL2) is a vital chemokine that mediates inflammation in Alzheimer’s disease (AD). We analyzed the associations between the baseline plasma MCP-1 level, longitudinal cognitive changes, and genetic effects of CCL2 rs1024611 and its receptor, CC-chemokine receptor 2 (CCR2) rs1799864, in AD. In total, 310 AD patients and 66 mild cognitive impairment (MCI) patients were followed for 2 years, and 120 controls were recruited at baseline for comparison. After adjusting for covariates using one-way analysis of covariance, AD patients had higher plasma MCP-1 levels compared with MCI patients and controls, and severe AD patients had the highest levels. After adjusting for covariates using generalized estimating equation analysis, the results showed that the baseline MCP-1 level was significantly correlated with changes in the two-year Mini-Mental Status Examination (p = 0.046). The A allele of CCR2 rs1799864 was associated with a higher MCP-1 level in AD and MCI patients. In conclusion, plasma MCP-1 might reflect the risk and disease course of AD. A higher plasma MCP-1 level is associated with greater severity and faster cognitive decline. Additionally, the CCR2 polymorphism may play a role in the regulation of MCP-1/CCR2 signaling in AD. Nature Publishing Group UK 2018-01-19 /pmc/articles/PMC5775300/ /pubmed/29352259 http://dx.doi.org/10.1038/s41598-018-19807-y Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Lee, Wei-Ju
Liao, Yi-Chu
Wang, Yen-Feng
Lin, I-Feng
Wang, Shuu-Jiun
Fuh, Jong-Ling
Plasma MCP-1 and Cognitive Decline in Patients with Alzheimer’s Disease and Mild Cognitive Impairment: A Two-year Follow-up Study
title Plasma MCP-1 and Cognitive Decline in Patients with Alzheimer’s Disease and Mild Cognitive Impairment: A Two-year Follow-up Study
title_full Plasma MCP-1 and Cognitive Decline in Patients with Alzheimer’s Disease and Mild Cognitive Impairment: A Two-year Follow-up Study
title_fullStr Plasma MCP-1 and Cognitive Decline in Patients with Alzheimer’s Disease and Mild Cognitive Impairment: A Two-year Follow-up Study
title_full_unstemmed Plasma MCP-1 and Cognitive Decline in Patients with Alzheimer’s Disease and Mild Cognitive Impairment: A Two-year Follow-up Study
title_short Plasma MCP-1 and Cognitive Decline in Patients with Alzheimer’s Disease and Mild Cognitive Impairment: A Two-year Follow-up Study
title_sort plasma mcp-1 and cognitive decline in patients with alzheimer’s disease and mild cognitive impairment: a two-year follow-up study
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5775300/
https://www.ncbi.nlm.nih.gov/pubmed/29352259
http://dx.doi.org/10.1038/s41598-018-19807-y
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