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

被引：255

作者：

Holmes, C ^{[1
]}

El-Okl, M ^{[1
]}

Williams, AL ^{[1
]}

Cunningham, C ^{[1
]}

Wilcockson, D ^{[1
]}

Perry, VH ^{[1
]}

机构：

[1] Univ Southampton, Sch Biol & Med Sci, Southampton, Hants, England

来源：

JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY | 2003年 / 74卷 / 06期

关键词：

D O I：

10.1136/jnnp.74.6.788

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

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.

引用

页码：788 / 789

页数：2

共 8 条

[1] Comparison of systemic cytokine levels in patients with acute respiratory distress syndrome, severe pneumonia, and controls [J].