On the relation of oxidative stress to neuroinflammation: lessons learned from the G93A-SOD1 mouse model of amyotrophic lateral sclerosis.

On the relation of oxidative stress to neuroinflammation: lessons learned from the G93A-SOD1 mouse model of amyotrophic lateral sclerosis. Research Abstract Details 

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On the relation of oxidative stress to neuroinflammation: lessons learned from the G93A-SOD1 mouse model of amyotrophic lateral sclerosis. Abstract Text:

Kenneth Hensley,Molina Mhatre,Shenyun Mou,Quentin N Pye,Charles Stewart,Melinda West,Kelly S Williamson,

The central nervous system (CNS) presents both challenges and opportunities to researchers of redox biochemistry. The CNS is sensitive to oxidative damage during aging or disease; excellent transgenic models of specific neurodegenerative diseases have been created that reproduce oxidative stress components of the corresponding human disorder. Mouse models of familial amyotrophic lateral sclerosis (ALS) based on overexpressed mutant human Cu, Zn-superoxide dismutase (SOD1) are cases in point. These animals experience predictably staged, age-dependent motor neuron degeneration with profound cellular and biochemical damage to nerve fibers and spinal cord tissue. Severe protein and lipid oxidation occurs in these animals, apparently as an indirect consequence of protein aggregation or cytopathic protein-protein interactions, as opposed to aberrant redox catalysis by the mutant enzyme. Recent studies of G93A-SOD1 mice and rats suggest that oxidative damage is part of an unmitigated neuroinflammatory reaction, possibly arising in combination from mitochondrial dysfunction plus pathophysiologic activation of both astrocytes and microglia. Lesions to redox signal-transduction pathways in mutant SOD1+ glial cells may stimulate broad-spectrum upregulation of proinflammatory genes, including arachidonic acid-metabolizing enzymes [e.g., cyclooxygenase-II (COX-II) and 5-lipoxygenase (5LOX)]; nitric oxide synthase (NOS) isoforms; cytokines (particularly tumor necrosis factor alpha, TNF-alpha); chemokines; and immunoglobulin Fc receptors (FcgammaRs). The integration of these processes creates a paracrine milieu inconsistent with healthy neural function. This review summarizes what has been learned to date from studies of mutant SOD1 transgenic animals and demonstrates that the G93A-SOD1 mouse in particular is a robust laboratory for the study of neuroinflammation and redox biochemistry.

On the relation of oxidative stress to neuroinflammation: lessons learned from the G93A-SOD1 mouse model of amyotrophic lateral sclerosis. Publishing Authors By Initials

K Hensley,M Mhatre,S Mou,QN Pye,C Stewart,M West,KS Williamson,

For similar enzymes and coenzymes: enzymes: oxidoreductases: superoxide dismutase research abstracts see: enzymes and coenzymes: enzymes: oxidoreductases: superoxide dismutase research

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On the relation of oxidative stress to neuroinflammation: lessons learned from the G93A-SOD1 mouse model of amyotrophic lateral sclerosis. Journal Published:

PUBLICATION TYPE: Review

Journal: Antioxidants & redox signaling

VOLUME: 8

Page Numbers: 2075-87

Journal Abbreviation: Antioxid. Redox Signal.

ISSN: 1523-0864

DAY: 3

MONTH: 12

YEAR: 2007

On the relation of oxidative stress to neuroinflammation: lessons learned from the G93A-SOD1 mouse model of amyotrophic lateral sclerosis. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100888899

On the relation of oxidative stress to neuroinflammation: lessons learned from the G93A-SOD1 mouse model of amyotrophic lateral sclerosis. Keywords Mesh Terms:

KEYWORDS: Superoxide Dismutase

MESH TERMS: genetics

Chemical & Substance for Abstract: On the relation of oxidative stress to neuroinflammation: lessons learned from the G93A-SOD1 mouse model of amyotrophic lateral sclerosis. Information

Substance Name: Superoxide Dismutase

Registry Number: EC 1.15.1.1

Grant and Affiliation Information for On the relation of oxidative stress to neuroinflammation: lessons learned from the G93A-SOD1 mouse model of amyotrophic lateral sclerosis.

AFFILIATION: Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland, USA. Kenneth-Hensley@omrf.ouhsc.edu

Country: United States

AGENCY: United States NINDS

GRANT: NS044154

ACRONYM: NS

MEDLINETA: Antioxid Redox Signal

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