Systemic infection, interleukin 1beta, and cognitive decline in Alzheimer's disease
Systemic infection, interleukin 1beta, and cognitive decline in Alzheimer's disease
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.
systemic infection, cytokine, alzheimers disease
788-789
Holmes, C.
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El-Okl, M.
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Williams, A.L.
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Cunningham, C.
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Wilcockson, D.
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Perry, V.H.
8f29d36a-8e1f-4082-8700-09483bbaeae4
June 2003
Holmes, C.
ada5abf3-8459-4cf7-be40-3f4e9391cc96
El-Okl, M.
9e426672-a3de-463a-bf9b-4631a9458ef3
Williams, A.L.
e3a98f1d-13e1-402e-a2a4-16a2d4acb898
Cunningham, C.
6d675038-a4b1-46e2-9e4b-0a5ac27ea2b2
Wilcockson, D.
5d01a633-d527-448f-8c41-141b3bef250c
Perry, V.H.
8f29d36a-8e1f-4082-8700-09483bbaeae4
Holmes, C., El-Okl, M., Williams, A.L., Cunningham, C., Wilcockson, D. and Perry, V.H.
(2003)
Systemic infection, interleukin 1beta, and cognitive decline in Alzheimer's disease.
Journal of Neurology Neurosurgery and Psychiatry, 74 (6), .
(doi:10.1136/jnnp.74.6.788).
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.
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Published date: June 2003
Keywords:
systemic infection, cytokine, alzheimers disease
Identifiers
Local EPrints ID: 27597
URI: http://eprints.soton.ac.uk/id/eprint/27597
ISSN: 0022-3050
PURE UUID: 56174878-5312-47f7-8baf-15b47879f601
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Date deposited: 26 Apr 2006
Last modified: 16 Mar 2024 03:06
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Author:
M. El-Okl
Author:
A.L. Williams
Author:
C. Cunningham
Author:
D. Wilcockson
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