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Preface; Contents; Contributors; Chapter 1: Mitochondrial ROS andßApoptosis; 1.1 Reactive Oxygen Species andßMitochondrial Sources ofßTheir Generation; 1.2 Mitochondrial Redox Systems; 1.2.1 The Mitochondrial GSH andßGlutathione-Dependent Enzymes; 1.2.2 Mitochondrial Thioredoxin andßThioredoxin-Dependent Enzymes; 1.3 Overview ofßApoptosis Pathways; 1.3.1 Receptor-Mediated (Extrinsic) Apoptosis; 1.3.2 Mitochondria-Derived (Intrinsic) Apoptosis; 1.4 Mitochondrial ROS (mtROS) andßImplication forßIntrinsic Apoptosis.
1.4.1 Cardiolipin Peroxidation andßInitiation ofßMitochondrial Apoptotic Signaling1.5 Role ofßMitochondrial GSH inßOxidant-Induced Intrinsic Apoptosis; 1.5.1 Mitochondrial GSH andßMitochondrial DNA Damage-ƯInduced Apoptosis; 1.6 Trx2 andßIntrinsic Apoptosis; 1.7 MtROS andßNeurodegenerative Disorders; 1.8 Summary andßPerspective; References; Chapter 2: Dopamine Metabolism andßReactive Oxygen Species Production; 2.1 Dopamine Metabolism; 2.1.1 Dopamine Biosynthesis; 2.1.2 Dopamine Degradation; 2.2 The Role ofßNeuromelanin inßDopaminergic Neurons; 2.3 ROS Production During Dopamine Metabolism.
2.3.1 MAO-Linked ROS Production2.3.2 Autoxidation-Linked ROS Production; 2.3.3 Permeability Transition Pores (PTPs); 2.3.4 l-DOPA Toxicity; 2.4 Astrocyte-Neuron Interactions; 2.5 Genetic andßEnvironmental Factors Affecting DA Metabolism; 2.5.1 Genetic Factors; 2.5.1.1 TH Deficiency; 2.5.1.2 DAT Genetic Variants; 2.5.2 Environmental Factors; 2.6 Summary; References; Chapter 3: The Consequences ofßDamaged Mitochondrial DNA; 3.1 Introduction ofßMitochondrial DNA; 3.1.1 MtDNA Structure; 3.1.2 MtDNA Gene Composition; 3.2 Mutations inßmtDNA; 3.2.1 Oxidative-Induced mtDNA Mutation.
3.2.2 Other Factors inßmtDNA Mutation3.3 MtDNA Maintenance andßRepair; 3.3.1 MtDNA Repair Mechanism-Base Excision Repair (BER); 3.3.2 Other Mechanisms Involved inßmtDNA Repair; 3.4 Damaged mtDNA Contributes toßMultiple Cellular Alterations; 3.4.1 Impaired Protein Synthesis andßFunction; 3.4.2 Decreased ATP Bioenergetics; 3.4.3 Nuclear Transcriptional Responses toßMitochondrial Defects; 3.5 MtDNA-Related (Mitochondrial) Diseases; 3.5.1 Common Mitochondrial Diseases; 3.5.2 Neurodegeneration andßmtDNA Mutations; 3.6 Potential Treatment Options; 3.7 Conclusion; References.
Chapter 4: The Role ofßChronic Inflammation inßtheßEtiology ofßParkinson's Disease4.1 Introduction; 4.1.1 Inflammation andßPD; 4.2 Parkinson Genes andßInflammation; 4.3 Inflammation andßToxin Animal Model ofßPD; 4.3.1 Toxin-Mediated Animal Model; 4.3.2 Inflammatory Mediated Animal Model; 4.4 Anti-inflammatory Treatment andßPD; 4.5 Conclusion; References; Chapter 5: Ion-Catalyzed Reactive Oxygen Species inßSporadic Models ofßParkinson's Disease; 5.1 Introduction; 5.1.1 Sporadic vs. Familial PD; 5.1.2 Etiology of PD; 5.1.3 Current Treatments; 5.2 Oxidative Stress andßAging Brain
5.3 Sources ofßROS inßDopaminergic Neurons.
1.4.1 Cardiolipin Peroxidation andßInitiation ofßMitochondrial Apoptotic Signaling1.5 Role ofßMitochondrial GSH inßOxidant-Induced Intrinsic Apoptosis; 1.5.1 Mitochondrial GSH andßMitochondrial DNA Damage-ƯInduced Apoptosis; 1.6 Trx2 andßIntrinsic Apoptosis; 1.7 MtROS andßNeurodegenerative Disorders; 1.8 Summary andßPerspective; References; Chapter 2: Dopamine Metabolism andßReactive Oxygen Species Production; 2.1 Dopamine Metabolism; 2.1.1 Dopamine Biosynthesis; 2.1.2 Dopamine Degradation; 2.2 The Role ofßNeuromelanin inßDopaminergic Neurons; 2.3 ROS Production During Dopamine Metabolism.
2.3.1 MAO-Linked ROS Production2.3.2 Autoxidation-Linked ROS Production; 2.3.3 Permeability Transition Pores (PTPs); 2.3.4 l-DOPA Toxicity; 2.4 Astrocyte-Neuron Interactions; 2.5 Genetic andßEnvironmental Factors Affecting DA Metabolism; 2.5.1 Genetic Factors; 2.5.1.1 TH Deficiency; 2.5.1.2 DAT Genetic Variants; 2.5.2 Environmental Factors; 2.6 Summary; References; Chapter 3: The Consequences ofßDamaged Mitochondrial DNA; 3.1 Introduction ofßMitochondrial DNA; 3.1.1 MtDNA Structure; 3.1.2 MtDNA Gene Composition; 3.2 Mutations inßmtDNA; 3.2.1 Oxidative-Induced mtDNA Mutation.
3.2.2 Other Factors inßmtDNA Mutation3.3 MtDNA Maintenance andßRepair; 3.3.1 MtDNA Repair Mechanism-Base Excision Repair (BER); 3.3.2 Other Mechanisms Involved inßmtDNA Repair; 3.4 Damaged mtDNA Contributes toßMultiple Cellular Alterations; 3.4.1 Impaired Protein Synthesis andßFunction; 3.4.2 Decreased ATP Bioenergetics; 3.4.3 Nuclear Transcriptional Responses toßMitochondrial Defects; 3.5 MtDNA-Related (Mitochondrial) Diseases; 3.5.1 Common Mitochondrial Diseases; 3.5.2 Neurodegeneration andßmtDNA Mutations; 3.6 Potential Treatment Options; 3.7 Conclusion; References.
Chapter 4: The Role ofßChronic Inflammation inßtheßEtiology ofßParkinson's Disease4.1 Introduction; 4.1.1 Inflammation andßPD; 4.2 Parkinson Genes andßInflammation; 4.3 Inflammation andßToxin Animal Model ofßPD; 4.3.1 Toxin-Mediated Animal Model; 4.3.2 Inflammatory Mediated Animal Model; 4.4 Anti-inflammatory Treatment andßPD; 4.5 Conclusion; References; Chapter 5: Ion-Catalyzed Reactive Oxygen Species inßSporadic Models ofßParkinson's Disease; 5.1 Introduction; 5.1.1 Sporadic vs. Familial PD; 5.1.2 Etiology of PD; 5.1.3 Current Treatments; 5.2 Oxidative Stress andßAging Brain
5.3 Sources ofßROS inßDopaminergic Neurons.