CCR3
趋化因子
CCR1
炎症
CCR10
CCL13型
趋化因子受体
免疫学
CCL7型
CCL11型
早老素
受体
生物
CCR2型
CXCL2型
淀粉样前体蛋白
阿尔茨海默病
四氯化碳
医学
内科学
疾病
生物化学
作者
Adrián Jordá,Martı́n Aldasoro,Constanza Aldasoro,Soraya L. Vallés
摘要
In Alzheimer's disease (AD), an increase in inflammation is distinctive. Amyloid precursor protein plus presenilin-1 (APP/PS1 mice) is a model for this illness. Chemokines secreted by central nervous system (CNS) cells could play multiple important roles in AD. Data looking for the chemokines involved in inflammatory mechanisms are lacking. To understand the changes that occur in the inflammation process in AD, it is necessary to improve strategies to act on specific inflammatory targets.Chemokines and their receptors involved in phagocytosis, demyelination, chemotaxis, and coagulation were the objective of our study.Female APPswe/PS1 double-transgenic mice (B6C3-Tg) were used and cortex brain from 20-22-month-old mice obtained and used to quantify chemokines and chemokine receptors expression using RT-PCR technique.Significant inflammatory changes were detected in APP/PS1 compared to wild type mice. CCR1, CCR3, CCR4, and CCR9 were elevated, and CCR2 were decreased compared with wild type mice. Their ligands CCL7, CCL11, CCL17, CCL22, CCL25, and CXCL4 showed an increase expression; however, changes were not observed in CCL2 in APP/PS1 compared to wild type mice.This change in expression could explain the differences between AD patients and elderly people without this illness. This would provide a new strategy for the treatment of AD, with the possibility to act in specific inflammatory targets.
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