Oxidative stress and redox signalling in Parkinson disease 1st Edition by Rodrigo Franco ISBN 9781788011914 1788011910

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ISBN 10: 1788011910
ISBN 13: 9781788011914
Author: Rodrigo Franco

Oxidative stress and redox signalling in Parkinson disease 1st Edition Table of 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

1.3.3 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 Pesticides

1.5.2 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

2.3 What Makes the Dopaminergic Neurons in the SNpc Vulnerable?

2.3.1 Cellular Organization of the SNpc

2.3.2 Redox Basis of the Vulnerability of SNpc DAergic Neurons

2.4 Conclusions and Perspectives

Acknowledgements

References

CHAPTER 3 Mitochondrial Dysfunction in Parkinson’s Disease

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

3.4.2 Rotenone: A Case for Complex I Inhibition

3.4.3 Paraquat: 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

4.1 The Life of Dopamine: Synthesis, Storage and Metabolism

4.2 3,4-Dihydroxyphenylacetaldehyde (DOPAL) and Biogenic Aldehydes Derived from Neurotransmitters

4.3 Generation of DOPAL and Biogenic Aldehydes at Aberrant Levels

4.3.1 Mechanisms for Elevation of DOPAL

4.3.2 Relevance of Altered Dopamine Metabolism/Trafficking to PD

4.4 Toxicity and Protein Reactivity of DOPAL and Biogenic Aldehydes

4.4.1 Mechanisms of Toxicity

4.4.2 Protein Reactivity and Targets

4.5 The Role of Biogenic Aldehydes in Disease

4.6 Summary

References

CHAPTER 5 Dopamine Oxidation and Parkinson’s Disease

5.1 Oxidative Stress and Susceptibility of Dopaminergic Neurons in Parkinson’s Disease

5.2 Dopamine Regulation and Metabolism

5.3 Pathological Dopamine Oxidation

5.3.1 Metabolism of Dopamine by Monoamine Oxidase

5.3.2 Oxidation of the Catechol Ring of Dopamine

5.3.3 Modification of Protein by Oxidized Dopamine

5.3.4 Mitochondrial Dysfunction and Dopamine Oxidation

5.4 The Role of Dopamine in Toxin-Induced Toxicity

5.5 Dopamine Toxicity

5.5.1 In vitro Exogenous Dopamine and l-DOPA Treatment

5.5.2 Exogenous Dopamine Administration in vivo

5.5.3 Dysregulation of Dopamine Handling in vivo

5.6 Dopamine and α-Synuclein

5.7 Dopamine Storage Disruption in PD

5.8 Summary and Conclusions

References

CHAPTER 6 Glutathione and Thiol Redox Signalling in Parkinson’s Disease

6.1 Introduction

6.2 Glutathione

6.3 Thiol Redox Signalling and Thiol–Disulfide Exchange

6.4 Cellular Reductases

6.4.1 Thioredoxins

6.4.2 Glutaredoxins

6.4.3 Peroxiredoxins

6.5 Glutathione Synthesis in the Brain

6.6 Glutathione and Models of Oxidative Stress in Dopaminergic Neurons

6.7 Glutathione Conjugating Enzymes

6.7.1 Glutathione Peroxidase

6.7.2 Glutathione S-Transferases

6.8 GSH and Transport in the Brain: Multidrug Resistance Proteins (MDRP) and the Blood–Brain Barrier (BBB)

6.9 Parkinson’s Disease Genetic Models and Redox Signalling

6.9.1 Glutathione-S-Transferase

6.9.2 DJ-1

6.9.3 PTEN-Induced Putative Kinase 1 (PINK1)

6.9.4 Parkin

6.10 Free Radicals as Messengers to Modulate Transcription Factors: Effects on Thiol Redox Regulation

6.11 Conclusions

References

CHAPTER 7 Neuroinflammation and Oxidative Stress in Models of Parkinson’s Disease and Protein-Misfolding Disorders

7.1 Introduction

7.2 Molecular Pathways Regulating Neuroinflammation in Glial Cells

7.2.1 Regulation of Inflammatory Genes in Glial Cells by NF-κB

7.2.2 Nuclear Regulation of NF-κB Function in Glial Cells

7.3 Neurotoxic Models of Parkinson’s Disease: Reactive Oxygen Species and Neuroinflammatory Mechanisms

7.3.1 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP)

7.3.2 6-Hydroxydopamine (6-OHDA)

7.3.3 Lipopolysaccharide (LPS)

7.4 Neuroinflammation and Protein Aggregation in PD and Protein-Misfolding Disorders

7.4.1 Neuroinflammation in Protein-Misfolding Disorders

7.4.2 Oxidative Stress in Protein-Misfolding Disorders

7.4.3 Unfolded Protein Response in Protein-Misfolding Disorders

7.5 Conclusions

References

CHAPTER 8 Redox Signalling in Dopaminergic Cell Death and Survival

8.1 Neuronal Degeneration in Parkinson’s Disease

8.1.1 Relatively Selective Dopaminergic Degeneration

8.1.2 Sources of Oxidative Stress and Selective Vulnerability

8.1.3 Increased Oxidative Stress and Selective Cell Death

8.2 Redox Signalling and Cell Survival/Death

8.3 Redox Regulation of DAergic Cell-Survival Pathways

8.3.1 Akt Structure and Function

8.3.2 Evidence of Akt1 Involvement in PD

8.3.3 Redox Regulation of Akt1 Activity

8.4 Redox Regulation of DAergic Cell-Death Pathways

8.4.1 Redox Regulation of MAP3K-ASK1

8.4.2 MAPKs – p38 and JNK

8.5 Conclusions

Acknowledgements

References

CHAPTER 9 Iron Metabolism in Parkinson’s Disease

9.1 Brain Iron Homeostasis

9.1.1 Brain Iron Transport and Distribution

9.1.2 Regulation of Brain Iron Homeostasis

9.2 Iron Metabolism and Parkinson’s Disease

9.2.1 Symptoms of Parkinson’s Disease

9.2.2 Iron Accumulation Accelerates the Symptomatology of Parkinson’s Disease

9.2.3 Mechanism of Iron Accumulation in the Substantia Nigra of Parkinson’s Disease Brains

9.2.4 Iron and the Aggregation of α-Synuclein

9.2.5 Iron, ROS and Apoptosis of Dopaminergic Neurons in the Substantia Nigra of Parkinson’s Disease

9.3 Iron-Related Therapeutic Approaches for PD

9.4 Conclusions

References

CHAPTER 10 Protein Oxidation, Quality-Control Mechanisms and Parkinson’s Disease

10.1 Introduction

10.2 Misfolded Protein Aggregation and Accumulation in PD

10.2.1 α-Synuclein: Mutations and Misfolding

10.3 Protein Quality-Control Mechanisms in PD

10.3.1 Protein Synthesis

10.3.2 Protein Folding, Unfolding and Disaggregation by Chaperones

10.3.3 Protein Degradation Pathways

10.3.4 Protein Quality Control in Organelles

10.4 Conclusions and Perspectives

Acknowledgements

References

CHAPTER 11 At the Intersection Between Mitochondrial Dysfunction and Lysosomal Autophagy: Role of PD-Related Neurotoxins and Gene Products

11.1 Introduction

11.2 Neuropathological Evidence for Mitochondrial Deficits and Autophagic Impairment in PD

11.2.1 Evidence of Mitochondrial Deficits in Postmortem PD Brains

11.2.2 Evidence of Autophagic Impairment in Postmortem PD Brains

11.3 Toxicological Evidence for Mitochondrial Deficits and Autophagic Impairment in PD

11.3.1 Rotenone

11.3.2 PQ and Maneb

11.3.3 MPTP or MPP+

11.3.4 6-OHDA

11.4 Genetic Evidence for Mitochondrial Deficits and Autophagic Impairment in PD

11.4.1 aSyn

11.4.2 Parkin/PINK1

11.4.3 DJ-1

11.4.4 ATP13A2

11.5 Interrelationships Between Autophagic Impairment and Mitochondrial Dysfunction

11.6 Summary and Future Directions

References

CHAPTER 12 Genes, Aging, and Parkinson’s Disease

12.1 Introduction

12.1.1 Do Genes Influence Lifespan?

12.1.2 Which Genes Influence Lifespan?

12.2 Apolipoprotein E

12.2.1 LDL Receptors

12.2.2 Effects of Polymorphisms on APOE Function

12.2.3 APOE and Parkinson’s Disease

12.2.4 APOE Oxidative Stress

12.3 FOXO3A and FOXO Family

12.3.1 FOXO3A Biological Functions

12.3.2 FOXO3A and Protein Homeostasis

12.3.3 FOXO3A and Parkinson’s Disease

12.4 Role of Other Genes Emerged from Animal Studies in Aging

12.4.1 Are Aging-Modifying Genes Discovered in Laboratory Animals Relevant for PD?

References

CHAPTER 13 Biomarkers of Oxidative Stress in Parkinson’s Disease

13.1 Biomarkers

13.2 Oxidative Stress

13.3 Candidate Biomarkers for ROS-Induced Stress

13.3.1 Halogenation

13.3.2 Methionine Oxidation

13.3.3 Glycation and Carbonylation

13.4 Candidate Biomarkers for RNS-Induced Stress

13.4.1 Nitration

13.4.2 S-nitros(yl)ation

13.5 Conclusions

References

CHAPTER 14 Dietary Anti-, Pro-Oxidants in the Etiology of Parkinson’s Disease

14.1 Introduction

14.2 Heterocyclic Amines

14.3 Polyphenolic Compounds

14.3.1 Flavonoids

14.3.2 Non-Flavonoids

14.4 Vitamins

14.4.1 Vitamin A

14.4.2 Vitamin B

14.4.3 Vitamin C

14.4.4 Vitamin D

14.4.5 Vitamin E

14.5 Summary

References

Subject Index

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