Does neuroinflammation fan the flame in neurodegenerative diseases?

<p>Abstract</p> <p>While peripheral immune access to the central nervous system (CNS) is restricted and tightly controlled, the CNS is capable of dynamic immune and inflammatory responses to a variety of insults. Infections, trauma, stroke, toxins and other stimuli are capable of p...

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Main Authors: McAlpine Fiona E, Alto Laura T, Frank-Cannon Tamy C, Tansey Malú G
Format: Article
Language:English
Published: BMC 2009-11-01
Series:Molecular Neurodegeneration
Online Access:http://www.molecularneurodegeneration.com/content/4/1/47
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author McAlpine Fiona E
Alto Laura T
Frank-Cannon Tamy C
Tansey Malú G
author_facet McAlpine Fiona E
Alto Laura T
Frank-Cannon Tamy C
Tansey Malú G
author_sort McAlpine Fiona E
collection DOAJ
description <p>Abstract</p> <p>While peripheral immune access to the central nervous system (CNS) is restricted and tightly controlled, the CNS is capable of dynamic immune and inflammatory responses to a variety of insults. Infections, trauma, stroke, toxins and other stimuli are capable of producing an immediate and short lived activation of the innate immune system within the CNS. This acute neuroinflammatory response includes activation of the resident immune cells (microglia) resulting in a phagocytic phenotype and the release of inflammatory mediators such as cytokines and chemokines. While an acute insult may trigger oxidative and nitrosative stress, it is typically short-lived and unlikely to be detrimental to long-term neuronal survival. In contrast, chronic neuroinflammation is a long-standing and often self-perpetuating neuroinflammatory response that persists long after an initial injury or insult. Chronic neuroinflammation includes not only long-standing activation of microglia and subsequent sustained release of inflammatory mediators, but also the resulting increased oxidative and nitrosative stress. The sustained release of inflammatory mediators works to perpetuate the inflammatory cycle, activating additional microglia, promoting their proliferation, and resulting in further release of inflammatory factors. Neurodegenerative CNS disorders, including multiple sclerosis (MS), Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), tauopathies, and age-related macular degeneration (ARMD), are associated with chronic neuroinflammation and elevated levels of several cytokines. Here we review the hallmarks of acute and chronic inflammatory responses in the CNS, the reasons why microglial activation represents a convergence point for diverse stimuli that may promote or compromise neuronal survival, and the epidemiologic, pharmacologic and genetic evidence implicating neuroinflammation in the pathophysiology of several neurodegenerative diseases.</p>
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spelling doaj.art-d639fc9c012444b6939b21c34342dd4a2022-12-22T02:59:21ZengBMCMolecular Neurodegeneration1750-13262009-11-01414710.1186/1750-1326-4-47Does neuroinflammation fan the flame in neurodegenerative diseases?McAlpine Fiona EAlto Laura TFrank-Cannon Tamy CTansey Malú G<p>Abstract</p> <p>While peripheral immune access to the central nervous system (CNS) is restricted and tightly controlled, the CNS is capable of dynamic immune and inflammatory responses to a variety of insults. Infections, trauma, stroke, toxins and other stimuli are capable of producing an immediate and short lived activation of the innate immune system within the CNS. This acute neuroinflammatory response includes activation of the resident immune cells (microglia) resulting in a phagocytic phenotype and the release of inflammatory mediators such as cytokines and chemokines. While an acute insult may trigger oxidative and nitrosative stress, it is typically short-lived and unlikely to be detrimental to long-term neuronal survival. In contrast, chronic neuroinflammation is a long-standing and often self-perpetuating neuroinflammatory response that persists long after an initial injury or insult. Chronic neuroinflammation includes not only long-standing activation of microglia and subsequent sustained release of inflammatory mediators, but also the resulting increased oxidative and nitrosative stress. The sustained release of inflammatory mediators works to perpetuate the inflammatory cycle, activating additional microglia, promoting their proliferation, and resulting in further release of inflammatory factors. Neurodegenerative CNS disorders, including multiple sclerosis (MS), Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), tauopathies, and age-related macular degeneration (ARMD), are associated with chronic neuroinflammation and elevated levels of several cytokines. Here we review the hallmarks of acute and chronic inflammatory responses in the CNS, the reasons why microglial activation represents a convergence point for diverse stimuli that may promote or compromise neuronal survival, and the epidemiologic, pharmacologic and genetic evidence implicating neuroinflammation in the pathophysiology of several neurodegenerative diseases.</p>http://www.molecularneurodegeneration.com/content/4/1/47
spellingShingle McAlpine Fiona E
Alto Laura T
Frank-Cannon Tamy C
Tansey Malú G
Does neuroinflammation fan the flame in neurodegenerative diseases?
Molecular Neurodegeneration
title Does neuroinflammation fan the flame in neurodegenerative diseases?
title_full Does neuroinflammation fan the flame in neurodegenerative diseases?
title_fullStr Does neuroinflammation fan the flame in neurodegenerative diseases?
title_full_unstemmed Does neuroinflammation fan the flame in neurodegenerative diseases?
title_short Does neuroinflammation fan the flame in neurodegenerative diseases?
title_sort does neuroinflammation fan the flame in neurodegenerative diseases
url http://www.molecularneurodegeneration.com/content/4/1/47
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