Review

The role of interleukin-1 in neuroinflammation and Alzheimer disease: an evolving perspective

Solomon S Shaftel¹ , W Sue T Griffin² and M Kerry O'Banion^1,3

¹  Department of Neurobiology and Anatomy, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA

²  Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA

³  Department of Neurology, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA

author email corresponding author email

Journal of Neuroinflammation 2008, 5:7doi:10.1186/1742-2094-5-7

Published:	26 February 2008

Abstract

Elevation of the proinflammatory cytokine Interleukin-1 (IL-1) is an integral part of the local tissue reaction to central nervous system (CNS) insult. The discovery of increased IL-1 levels in patients following acute injury and in chronic neurodegenerative disease laid the foundation for two decades of research that has provided important details regarding IL-1's biology and function in the CNS. IL-1 elevation is now recognized as a critical component of the brain's patterned response to insults, termed neuroinflammation, and of leukocyte recruitment to the CNS. These processes are believed to underlie IL-1's function in the setting of acute brain injury, where it has been ascribed potential roles in repair as well as in exacerbation of damage. Explorations of IL-1's role in chronic neurodegenerative disease have mainly focused on Alzheimer disease (AD), where indirect evidence has implicated it in disease pathogenesis. However, recent observations in animal models challenge earlier assumptions that IL-1 elevation and resulting neuroinflammatory processes play a purely detrimental role in AD, and prompt a need for new characterizations of IL-1 function. Potentially adaptive functions of IL-1 elevation in AD warrant further mechanistic studies, and provide evidence that enhancement of these effects may help to alleviate the pathologic burden of disease.