Abstract
A large body of evidence on brain development and ageing has revealed that inflammatory processes profoundly affect brain functions during life span of mammalians, including humans. Activation of innate immune mechanisms leading to pro-inflammatory cytokine up-regulation is involved in devastating and disabling human brain illnesses, as Alzheimers disease (AD), a progressive neurodegenerative disease that causes dementia in the elderly. Emerging data indicate that the cytokine Interleukin (IL)-18, one of the key mediator of inflammation and immune response, has relevance in the physiopathological processes of the brain, by ultimately influencing the integrity of neurons and putatively contributing to AD. In this review, the relationship between specific IL-18-mediated processes and AD neurodegeneration is summarized and clinical studies pointing to a role of the cytokine in the pathology are discussed. Altogether, the presented data indicate that a more complete knowledge of the molecular mechanisms underlying IL-18 implication in neuroinflammatory and neurodegenerative pathways could contribute toward the development of new therapeutic strategies for AD.
Keywords: Interleukin-18, Alzheimer's disease, neuroinflammation, cytokines
Current Pharmaceutical Design
Title: Interleukin-18, From Neuroinflammation to Alzheimers Disease
Volume: 16 Issue: 38
Author(s): Paola Bossu, Antonio Ciaramella, Francesca Salani, Diego Vanni, Ilaria Palladino, Carlo Caltagirone and Giuseppe Scapigliati
Affiliation:
Keywords: Interleukin-18, Alzheimer's disease, neuroinflammation, cytokines
Abstract: A large body of evidence on brain development and ageing has revealed that inflammatory processes profoundly affect brain functions during life span of mammalians, including humans. Activation of innate immune mechanisms leading to pro-inflammatory cytokine up-regulation is involved in devastating and disabling human brain illnesses, as Alzheimers disease (AD), a progressive neurodegenerative disease that causes dementia in the elderly. Emerging data indicate that the cytokine Interleukin (IL)-18, one of the key mediator of inflammation and immune response, has relevance in the physiopathological processes of the brain, by ultimately influencing the integrity of neurons and putatively contributing to AD. In this review, the relationship between specific IL-18-mediated processes and AD neurodegeneration is summarized and clinical studies pointing to a role of the cytokine in the pathology are discussed. Altogether, the presented data indicate that a more complete knowledge of the molecular mechanisms underlying IL-18 implication in neuroinflammatory and neurodegenerative pathways could contribute toward the development of new therapeutic strategies for AD.
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Cite this article as:
Bossu Paola, Ciaramella Antonio, Salani Francesca, Vanni Diego, Palladino Ilaria, Caltagirone Carlo and Scapigliati Giuseppe, Interleukin-18, From Neuroinflammation to Alzheimers Disease, Current Pharmaceutical Design 2010; 16 (38) . https://dx.doi.org/10.2174/138161210794519147
DOI https://dx.doi.org/10.2174/138161210794519147 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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