[Frontiers in Bioscience 3, c8-16, March 25, 98]

	[Frontiers in Bioscience 3, c8-16, March 25, 98] Reprints PubMed CAVEAT LECTOR
	USE OF GENETICALLY ENGINEERED MICE AS MODELS FOR EXPLORING THE ROLE OF OXIDATIVE STRESS IN NEURODEGENERATIVE DISEASES Julie K. Andersen Division of Biogerontology, Andrus Gerontology Center, University of Southern California, Los Angeles, CA 90089-0191 Received 3/16/98 Accepted 3/20/98 TABLE OF CONTENTS 1. Abstract 2. Introduction 3. Discussion 3.1. Amyotrophic Lateral Sclerosis (ALS) 3.1.1. Mutations in SOD are involved in some forms of ALS 3.1.2. Studies on genetically engineered mice containing human familial ALS SOD mutations 3.1.3. Free radical production in mutant ALS SOD-containing mouse lines 3.2. Parkinson’s Disease (PD) 3.2.1. MPTP toxicity as a model for PD 3.2.2. Use of genetically engineered mice to explore the role of ROS in MPTP toxicity 3.2.3. Glutathione may act to protect dopaminergic neurons against damage mediated by energy impairment: a possible factor in PD 3.3 Alzheimer’s Disease (AD) 3.3.1. Beta-amyloid and AD 3.3.2 ROS production as a causative agent in beta-amyloid induced neurotoxicity 3.3.3 Studies on genetically engineered mice with elevated Aß to investigate whether ROS is a component in its neurodegenerative effects in vivo 3.4. Huntington’s Disease (HD) 3.4.1 Excitotoxic model of HD 3.4.2. Use of genetically engineered mice to assess the part that ROS production may play in excitotoxic cell death 4. Conclusion 5. Acknowledgments 6. References 7. Entire manuscript Key words:Transgenic, Knock-Out, Neurodegerative Disease, Oxidative Stress Search OMIM (Online Mendelian Inheritance in Man) to find related articles This form requires a WWW Client such as Netscape, XMosaic, Lynx that supports fill-in forms. Enter one or more search keywords: To Search all fields, leave the following boxes unchecked. To narrow your search to certain specific fields, check the boxes next to those fields' names. SeeQuery Help for other ways to search. Title: OMIM Number: Allelic Variants: Text: References: Clinical Synopsis: Gene Map Disorder: Contributors: See only records which have been changed in the past Display at most

[Frontiers in Bioscience 3, c8-16, March 25, 98]
Reprints
PubMed
CAVEAT LECTOR

USE OF GENETICALLY ENGINEERED MICE AS MODELS FOR EXPLORING THE ROLE OF OXIDATIVE STRESS IN NEURODEGENERATIVE DISEASES

Julie K. Andersen

Division of Biogerontology, Andrus Gerontology Center, University of Southern California, Los Angeles, CA 90089-0191

Received 3/16/98 Accepted 3/20/98

TABLE OF CONTENTS


1. Abstract
2. Introduction
3. Discussion: 3.1. Amyotrophic Lateral Sclerosis (ALS)
3.1.1. Mutations in SOD are involved in some forms of ALS
3.1.2. Studies on genetically engineered mice containing human familial ALS SOD mutations
3.1.3. Free radical production in mutant ALS SOD-containing mouse lines

3.2. Parkinson’s Disease (PD)
3.2.1. MPTP toxicity as a model for PD
3.2.2. Use of genetically engineered mice to explore the role of ROS in MPTP toxicity
3.2.3. Glutathione may act to protect dopaminergic neurons against damage mediated by energy impairment: a possible factor in PD

3.3 Alzheimer’s Disease (AD)
3.3.1. Beta-amyloid and AD
3.3.2 ROS production as a causative agent in beta-amyloid induced neurotoxicity
3.3.3 Studies on genetically engineered mice with elevated Aß to investigate whether ROS is a component in its neurodegenerative effects in vivo

3.4. Huntington’s Disease (HD)
3.4.1 Excitotoxic model of HD
3.4.2. Use of genetically engineered mice to assess the part that ROS production may play in excitotoxic cell death
4. Conclusion
5. Acknowledgments
6. References
7. Entire manuscript

Key words:Transgenic, Knock-Out, Neurodegerative Disease, Oxidative Stress

Search OMIM (Online Mendelian Inheritance in Man) to find related articles
This form requires a WWW Client such as Netscape, XMosaic, Lynx that supports fill-in forms.