Systemic infection, interleukin 1β, and cognitive decline in Alzheimer’s disease
- Correspondence to: Dr Clive Holmes, University of Southampton, Clinical Neurosciences Research Division, Memory Assessment and Research Centre, Moorgreen Hospital, Botley Rd, West End, Southampton SO30 3JB, UK; ch4{at}soton.ac.uk
- Received 27 September 2002
- Accepted 21 December 2002
- Revised 12 December 2002
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 1β 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 1β. 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.
Footnotes
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Competing interests: none declared
