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

Shaftel SS, Griffin WS, O'Banion MK - J Neuroinflammation (2008)

Bottom Line: 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.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Neurobiology and Anatomy, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA. solomon_shaftel@urmc.rochester.edu

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.

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A schematic depiction of potential roles of IL-1 in AD.
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Figure 1: A schematic depiction of potential roles of IL-1 in AD.

Mentions: At the present time our understanding of the relationship between neuroinflammation, IL-1, and AD is evolving. The downstream consequences of IL-1 elevation in AD likely involve a balance between the beneficial and detrimental functions highlighted in this review (Figure 1). Failures of recent anti-inflammatory trials in the treatment of AD may be in part explained by blockade of both beneficial and detrimental neuroinflammatory processes in the course of disease. Current findings are consistent with the idea that strategies aimed at enhancing beneficial components of neuroinflammatory pathways in chronic neurodegenerative disease may hold promise in the development of new therapies.


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

Shaftel SS, Griffin WS, O'Banion MK - J Neuroinflammation (2008)

A schematic depiction of potential roles of IL-1 in AD.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2335091&req=5

Figure 1: A schematic depiction of potential roles of IL-1 in AD.
Mentions: At the present time our understanding of the relationship between neuroinflammation, IL-1, and AD is evolving. The downstream consequences of IL-1 elevation in AD likely involve a balance between the beneficial and detrimental functions highlighted in this review (Figure 1). Failures of recent anti-inflammatory trials in the treatment of AD may be in part explained by blockade of both beneficial and detrimental neuroinflammatory processes in the course of disease. Current findings are consistent with the idea that strategies aimed at enhancing beneficial components of neuroinflammatory pathways in chronic neurodegenerative disease may hold promise in the development of new therapies.

Bottom Line: 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.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Neurobiology and Anatomy, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA. solomon_shaftel@urmc.rochester.edu

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.

Show MeSH
Related in: MedlinePlus