Oxidative Tissue Injury in Experimental Models of Multiple Sclerosis

Cornelia Schuh

ISBN 10: 3838139356 / ISBN 13: 9783838139357

Published by Südwestdeutscher Verlag Für Hochschulschriften, 2015

About this Item

nach der Bestellung gedruckt Neuware - Printed after ordering - Multiple sclerosis (MS) is a chronic disease of the central nervous system. A number of different animal models of MS contributed to a better understanding of MS pathology. Additionally, experimental models enabled the development of immune-modulatory therapies for MS patients. In recent years, growing evidence for a major role of oxidative injury in demyelination and neurodegeneration in MS has been emerging. Hence, we aimed to characterise the nature and the extent of oxidative damage in different experimental models in comparison to MS. For this purpose, we emphasised the expression of enzymes involved in reactive species production and the accumulation of oxidised phospholipids and iron, which is a potential amplifier of oxidative damage. The different animal models were triggered by diverse inflammatory mechanisms, each representing distinct aspects of MS pathology. The presented study reports a diverging extent of oxidative injury and underlying mechanisms in different models for inflammatory demyelination.

Seller Inventory # 9783838139357

Bibliographic Details

• Title: Oxidative Tissue Injury in Experimental Models of Multiple Sclerosis
• Publisher: Südwestdeutscher Verlag Für Hochschulschriften
• Publication Date: 2015
• Language: English
• ISBN 10: 3838139356
• ISBN 13: 9783838139357
• Binding: Taschenbuch
• Condition: Neu
• Dimensions: 220W x 150H x 11D millimeters 220 millimeters width by 150 millimeters height by 11 millimeters depth
• Weight: 286 grams

About this title

Synopsis

Multiple sclerosis (MS) is a chronic disease of the central nervous system. A number of different animal models of MS contributed to a better understanding of MS pathology. Additionally, experimental models enabled the development of immune-modulatory therapies for MS patients. In recent years, growing evidence for a major role of oxidative injury in demyelination and neurodegeneration in MS has been emerging. Hence, we aimed to characterise the nature and the extent of oxidative damage in different experimental models in comparison to MS. For this purpose, we emphasised the expression of enzymes involved in reactive species production and the accumulation of oxidised phospholipids and iron, which is a potential amplifier of oxidative damage. The different animal models were triggered by diverse inflammatory mechanisms, each representing distinct aspects of MS pathology. The presented study reports a diverging extent of oxidative injury and underlying mechanisms in different models for inflammatory demyelination.