Oxidative stress and redox signalling in Parkinson's disease / editors: Rodrigo Franco, Jonathan A. Doorn, Jean-Christophe Rochet.
This book provides a thorough review of the latest research developments regarding the mechanisms by which oxidative stress and redox signalling mediate Parkinson's Disease.
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Full Text (via RSC) |
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| Other Authors: | , , |
| Format: | eBook |
| Language: | English |
| Published: |
[Cambridge] :
Royal Society of Chemistry,
[2018]
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| Series: | Issues in toxicology ;
34. |
| Subjects: |
Table of Contents:
- Cover; Oxidative Stress and Redox Signalling in Parkinson's Disease; Preface; Contents; Chapter 1
- Etiology and Pathogenesis of Parkinson's Disease; 1.1 Introduction; 1.2 Clinical Manifestations of Parkinson's Disease; 1.3 Neuropathology; 1.3.1 Selective Vulnerability of the Nigrostriatal Dopamine Neuron; 1.3.2 Mitochondrial Dysfunction in PD; 1.3.2.1 Mitochondrial DNA Damage; 1.3.2.2 Complex I Inhibition; 1.3.3 Oxidative Stress; 1.3.4 Dopamine Metabolism; 1.3.5 Neuroinflammation; 1.4 Genetics of Parkinson's Disease; 1.5 Environmental Exposures and the Risk of Parkinson's Disease.
- 1.5.1 Pesticides1.5.2 Metals; 1.5.3 Pathogens; 1.6 Gene-Environment Interaction; 1.7 Conclusions; Acknowledgements; References; Chapter 2
- Oxidative Stress and Redox Signalling in the Parkinson's Disease Brain; 2.1 Introduction; 2.2 Oxidative Stress and Antioxidant Systems; 2.2.1 Reactive Oxygen and Nitrogen Species: Sources; 2.2.2 Antioxidant Systems; 2.2.3 Oxidative Damage to Biomolecules; 2.2.3.1 Oxidative DNA Damage; 2.2.3.2 Oxidative Damage to Lipids; 2.2.3.3 Oxidative Protein Modifications: Redox Sensors and Transducers; 2.3 What Makes the Dopaminergic Neurons in the SNpc Vulnerable.
- 3.1 Reactive Oxygen Species (ROS)3.1.1 Mitochondria and ROS Production; 3.2 Parkinson's Disease; 3.3 Mitochondrial Dysfunction in PD; 3.3.1 ETC Complex Deficiency in PD; 3.3.2 Altered Mitochondrial Morphology; 3.3.3 Mitochondrial Ca2+ Buffering in PD; 3.3.4 PD-Related Genes and Mitochondrial Dysfunction; 3.4 Mitochondrial Dysfunction in Toxicant-Induced PD; 3.4.1 6-OHDA and MPTP: Classic Toxicant Models; 3.4.1.1 6-OHDA: An Experimental Catecholaminergic Neurotoxicant; 3.4.1.2 MPTP: Evidence for CI and the Toxic Exposure Hypothesis of PD; 3.4.2 Rotenone: A Case for Complex I Inhibition.
- 3.4.3 Paraquat: Redox Cycling Agent3.4.3.1 Characteristics and Risk of Exposure; 3.4.3.2 Mechanism of Toxicity: Redox Cycling and ROS Generation; 3.4.3.3 Role of Mitochondria in PQ Toxicity; 3.4.3.4 PQ and Excitotoxicity; 3.4.3.5 Using PQ for Developing Animal Models of PD; 3.4.3.6 Diquat Use with PQ: Example of Another Redox Cycling Agent; 3.4.4 Maneb: A Role of Complex III in PD Pathogenesis; 3.4.5 Other Environmental Toxins; 3.5 Concluding Remarks; References; Chapter 4
- Dopamine Metabolism and the Generation of a Reactive Aldehyde.