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全身感染、白细胞介素1β与阿尔茨海默病的认知衰退

Systemic infection, interleukin 1beta, and cognitive decline in Alzheimer's disease.

作者信息

Holmes C, El-Okl M, Williams A L, Cunningham C, Wilcockson D, Perry V H

机构信息

School of Medicine and Biological Sciences, University of Southampton, Southampton, UK.

出版信息

J Neurol Neurosurg Psychiatry. 2003 Jun;74(6):788-9. doi: 10.1136/jnnp.74.6.788.

DOI:10.1136/jnnp.74.6.788
PMID:12754353
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1738504/
Abstract

Activated microglia, the resident macrophages of the brain, are a feature of Alzheimer's disease. Animal models suggest that when activated microglia are further activated by a subsequent systemic infection this results in significantly raised levels of interleukin 1beta within the CNS, which may in turn potentiate neurodegeneration. This prospective pilot study in Alzheimer's disease subjects showed that cognitive function can be impaired for at least two months after the resolution of a systemic infection and that cognitive impairment is preceded by raised serum levels of interleukin 1beta. These relations were not confounded by the presence of any subsequent systemic infection or by baseline cognitive scores. Further research is needed to determine whether recurrent systemic infections drive cognitive decline in Alzheimer's disease subjects through a cytokine mediated pathway.

摘要

活化的小胶质细胞是大脑中的常驻巨噬细胞,是阿尔茨海默病的一个特征。动物模型表明,当活化的小胶质细胞被随后的全身感染进一步激活时,这会导致中枢神经系统内白细胞介素1β水平显著升高,进而可能增强神经退行性变。这项针对阿尔茨海默病患者的前瞻性初步研究表明,全身感染消退后,认知功能至少会受损两个月,且认知障碍之前血清白细胞介素1β水平会升高。这些关系不受任何随后的全身感染或基线认知评分的影响。需要进一步研究以确定复发性全身感染是否通过细胞因子介导的途径导致阿尔茨海默病患者认知能力下降。

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