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

• Published in: Journal of neurology, neurosurgery and psychiatry Vol. 74; no. 6; pp. 788 - 789
• Main Authors: Holmes, C, El-Okl, M, Williams, A L, Cunningham, C, Wilcockson, D, Perry, V H
• Format: Journal Article
• Language: English
• Published: London BMJ Publishing Group Ltd 01-06-2003; BMJ
• Subjects: Alzheimer's disease; Biological and medical sciences; Cognition disorders; Complications and side effects; cytokine; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Development and progression; Infection; Interleukin-1; Medical sciences; Neurology; Physiological aspects; Psychological aspects; systemic infection; United Kingdom; Human; Nervous system diseases; Cognitive disorder; Alzheimer disease; Pathogenesis; Cytokine; Interleukin 1β; Systemic; Cerebral disorder; Infection; Central nervous system disease; Serum; Degenerative disease; Elderly; Quantitative analysis
• ISSN: 0022-3050; 1468-330X
• DOI: 10.1136/jnnp.74.6.788

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.