Systemic infection, interleukin 1beta, and cognitive decline in Alzheimer's disease
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), 788-789. (doi:10.1136/jnnp.74.6.788).
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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.
|Digital Object Identifier (DOI):||doi:10.1136/jnnp.74.6.788|
|Keywords:||systemic infection, cytokine, alzheimers disease|
|Subjects:||R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry|
|Divisions:||University Structure - Pre August 2011 > School of Medicine > Clinical Neurosciences
|Date Deposited:||26 Apr 2006|
|Last Modified:||06 Aug 2015 02:28|
|RDF:||RDF+N-Triples, RDF+N3, RDF+XML, Browse.|
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