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Neuron-Glia Interaction in Neuroinflammation

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ISBN 10: 1461483123 / ISBN 13: 9781461483120
Published by Springer
New Condition: New Hardcover
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Hardcover. 187 pages. Dimensions: 9.2in. x 6.1in. x 0.6in.Accumulation on glia is an active pathological element in many neurological disorders. Gliosis produces neuroinflammation through both neurotrophic and inflammatory means, but the exact mechanism through which this happens remain unclear. It is suspected that damage to neurons activates the growth of glial cells. The proposed book focuses on the interaction between neurons and glia to help elucidate the pathophysiology of neuroinflammation in neurological disorders. This item ships from multiple locations. Your book may arrive from Roseburg,OR, La Vergne,TN. Bookseller Inventory # 9781461483120

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Bibliographic Details

Title: Neuron-Glia Interaction in Neuroinflammation

Publisher: Springer

Binding: Hardcover

Book Condition:New

Book Type: Hardcover

About this title

Synopsis:

Accumulation on glia is an active pathological element in many neurological disorders. Gliosis produces neuroinflammation through both neurotrophic and inflammatory means, but the exact mechanism through which this happens remain unclear. It is suspected that damage to neurons activates the growth of glial cells. The proposed book focuses on the interaction between neurons and glia to help elucidate the pathophysiology of neuroinflammation in neurological disorders.

From the Back Cover:

Accumulation of glia, gliosis, in various neurological disorders is not a static scar, but actively involved in pathogenesis of various neurological and psychiatric disorders, where glial cells produce both inflammatory and neurotrophic factors. These factors may play a role in neuronal damage, but also have a protective and reparative function by inducing neuroinflammation. However, definition as well as the mechanisms of neuroinflammation is not yet clear. We first define acute, chronic and non-classical neuroinflammation.

Glial cells are activated by a variety of stimuli via receptors on glial cells. Toll like receptors (TLR) are one of these receptors. In response to harmful stimuli, neurons produce factors as either “eat-me” or “help-me” signals. These factors include cytokines, chemokines and damage-associated molecular pattern (DAMP). Some of them activate glial cells via TLR, and function to protect neurons or further induce neuroinflammation. Thus, the interaction between neuron-glia and glia-glia is a main feature of neuroinflammation. Glial cells communicate with other glial or neural cells via gap-junctions. The communication may also be important for the understanding of neuroinflammation. Oligodendrocytes-neurons communication may be critical in either myelination or demyelination. Damage of blood-brain barrier (BBB) is common feature of both inflammatory and degenerative neurological disorders. Thus, relation of BBB damage and functions of glial cell may also be important in the development of neuroinflammation.

In this book, we focused on neuron-glia interaction of various aspects for understanding of pathophysiology of neuroinflammation in development of inflammatory as well as degenerative neurological disorders.

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