Generic placeholder image

Current Pharmaceutical Design

Editor-in-Chief

ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

Interleukin-18, From Neuroinflammation to Alzheimers Disease

Author(s): Paola Bossu, Antonio Ciaramella, Francesca Salani, Diego Vanni, Ilaria Palladino, Carlo Caltagirone and Giuseppe Scapigliati

Volume 16 , Issue 38 , 2010

Page: [4213 - 4224] Pages: 12

DOI: 10.2174/138161210794519147

Price: $65

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


Rights & Permissions Print Export Cite as
© 2022 Bentham Science Publishers | Privacy Policy