Systemic immune aberrations in Alzheimer's disease patients

被引:112
作者
Bonotis, Konstantinos [1 ]
Krikki, Eleni [1 ]
Holeva, Vasiliki [2 ]
Aggouridaki, Christina [3 ]
Costa, Vasiliki [1 ]
Baloyannis, Stavros [1 ]
机构
[1] Aristotle Univ Thessaloniki, Dept Neurol 1, Thessaloniki, Greece
[2] Aristotle Univ Thessaloniki, Dept Psychiat 1, Thessaloniki, Greece
[3] Aristotle Univ Thessaloniki, Dept Microbiol, Thessaloniki, Greece
关键词
immunological markers; cytokine; lymphocyte subpopulations; Alzheimer's disease; chronic inflammation;
D O I
10.1016/j.jneuroim.2007.10.020
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The role of chronic inflammation in the pathogenesis of Alzheimer's disease (AD) has been implied in a plethora of studies. The objective of the present study was to evaluate the immune alterations and the immunological markers in patients suffering from AD. IL-1 alpha, IL-2, IL-6, IL-8, IL-10, TNF-alpha cytokine and helper/inducer (CD4), suppressor/cytotoxic (CD8) T lymphocyte levels were investigated in patients with various degrees of cognitive impairment (mild-moderate and severe stage), as well as in age-matched non demented controls. Cytokines were measured using the ELISA immunoassay method and lymphocytes using flow cytometry. Results showed a significant TNF-a increase in patients of severe stage serum compared to controls as well as a significant decrease of CD4 lymphocyte subpopulation levels in patients of severe stage compared to those of mild-moderate stage patients and controls. No significant differences were observed on IL-1 alpha, IL-2, IL-6, IL-8, IL-10 cytokine levels and on CD8, CD4/CD8 lymphocyte subpopulations levels between patients and controls neither between mild moderate and severe stage patients. CD4 lymphocyte subpopulation and cytokine IL-2 were revealed as having a significant relationship (positive and negative respectively) with the MMSE score of patients. Data suggest the existence of detectable changes of peripheral immune system in AD. (C) 2007 Elsevier B.V. All rights reserved.
引用
收藏
页码:183 / 187
页数:5
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