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Chapter category: Protein

Tumor Necrosis Factor (TNF) and Neurodegeneration

This chapter appears in the following book:

TNF Superfamily

Edited by: Sanjay Khare
ISBN: 978-1-58706-306-0
» Get more information about this book at landesbioscience.com «

Chapter authors:
Rammohan V. Rao, H. Michael Ellerby and Dale E. Bredesen


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Cytokines are a family of growth factors that are secreted by the cells of the immune system. The family includes interleukins (IL), interferons (IFN), tumor necrosis factors (TNF), chemokines and other growth factors. Cytokines stimulate both the humoral and cellular immune responses as well as the activation of phagocytic cells and are generally associated with inflammation, immune activation, cell differentiation and cell death. They have diverse actions and are rapidly induced in response to tissue injury, infection or inflammation. Their role as mediators and inhibitors of diverse forms of neurodegeneration is increasingly recognized. Cytokines are induced in response to brain injury and can either induce, mediate, inhibit, or exacerbate cellular injury and repair. Several proinflammatory cytokines, notably tumor necrosis factor-a (TNF-a), have been shown to mediate diverse forms of experimental neurodegeneration, and both neurotoxic and neuroprotective actions have been reported. Here we review evidence for the contribution of cytokines to neurodegeneration, focusing primarily on tumor necrosis factor (TNF), which not only contributes to neuronal injury but may also exert protective effects. Since the mechanism of action of TNF and its interactions with various molecules in neurodegeneration is largely unknown, questions regarding these processes are of paramount importance to neurobiologists. Understanding the precise role of TNF in neurodegeneration is likely to have direct relevance in the search for potential treatments for neurodegenerative disease.

Rammohan V. Rao
Buck Institute for Age Research; University of California, San Francisco

H. Michael Ellerby
Buck Institute for Age Research

Dale E. Bredesen
Buck Institute for Age Research

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