Oxidative Stress And Redox Signalling In Parkinson S Disease

Parkinson's Disease is the second most common neurodegenerative disorder affecting millions of people worldwide. In order to find neuroprotective strategies, a clear understanding of the mechanisms involved in the dopaminergic death of cells that progresses the disease is needed. Oxidative stress can be defined as an imbalance between the production of reactive species and the ability to detoxify them and their intermediates or by-products. Oxidative damage to lipids, proteins, and DNA has been detected in autopsies from individuals with Parkinson’s Disease and so links can be made between oxidative stress and Parkinson’s Disease pathogenesis. This book provides a thorough review of the mechanisms by which oxidative stress and redox signalling mediate Parkinson’s Disease. Opening chapters bring readers up to speed on basic knowledge regarding oxidative stress and redox signalling, Parkinson’s Disease, and neurodegeneration before the latest advances in this field are explored in detail. Topics covered in the following chapters include the role of mitochondria, dopamine metabolism, metal homeostasis, inflammation, DNA-damage and thiol-signalling. The role of genetics and gene-environment interactions are also explored before final chapters discuss the identification of potential biomarkers for diagnosis and disease progression and the future of redox/antioxidant based therapeutics. Written by recognized experts in the field, this book will be a valuable source of information for postgraduate students and academics, clinicians, toxicologists and risk assessment groups. Importantly, it presents the current research that might later lead to redox or antioxidant – based therapeutics for Parkinson’s disease.

This book deals with basic and clinical aspects of monoamine oxidase (MAO) subtypes A and B highlighting its importance in neurological and psychiatric diseases. Consequently the therapeutic actions of MAO-A and -B inhibitors in Parkinson’s disease (PK) and depression are the focus of several chapters. As MAO is the basis of the development of the "oxidative stress hypothesis" of PD, several chapters are devoted to iron and iron-induced oxidative stress in various experimental studies and clinical conditions. Based on these findings, new compounds have been developed which not only block MAO, but are in addition, either inhibitors of acetylcholine esterase or have iron chelating properties. The aspect of "preclinical" and "clinical" neuro protection as well as MAO neuroprotection are additional topics covered in this book. MAO, iron and neuroprotection are seen in the framework of general anti Parkinson’s therapy with chapters on levodopa, dopaminergic receptor agonists and clinical issues.

This volume presents a unique comparative treatment of the role oxidative stress plays in vertebrates and invertebrates in multiple organ systems with regards to cell death, development, aging, and human diseases, and anti-oxidant therapy. It offers comprehensive reviews of the current understanding of oxidative stress-mediated physiology and pathology as well as directions for future research. It also provides current information on the role of oxidative stress in neurodegenerative diseases, cardiovascular diseases, and various types of cancer mediated by oxidative stress.

The role of free radicals and oxidative stress in neurological disorders has only recently been recognized, leaving clinical neurologists to seek in vain for information on the subject even in major textbooks. What published information there is may consist of brief reminders of the possible association of superoxidase dismutase with familial amyotrophic lateral sclerosis and nitrous oxide with migraine. With luck they may also find information on the purported role of free radicals in the pathogenesis of traumatic brain injury. Oxidative Stress and Free Radical Damage in Neurology sets the record straight, focusing on clinical and research issues regarding the interplay of free radicals and the human nervous system. Crucially, the chapters cover numerous antioxidants and their possible therapeutic role in neurological disorders. Key illnesses such as epilepsy, multiple sclerosis and Parkinson’s are analyzed, and chapters also examine more general issues such as the link between free radicals and inflammation of the central nervous system. Clinicians and laboratory researchers alike will find that this book augments their understanding not only of the widespread involvement of free radicals in the central nervous system but also of some uncertainties surrounding whether free radical damage in neurology plays a primary or secondary role.

Based on a conference on Oxidative Stress and Redox Regulation, held at the Pasteur Institute, Paris, this work examines fundamental, chemical, biological and medical studies of free radicals on different targets and the consequences of their reactivity. It covers the chemistry and biochemistry of free radicals, free radicals as second messengers t

Oxidative stress is the result of an imbalance in pro-oxidant/antioxidant homeostasis that leads to the generation of toxic reactive oxygen species. Brain cells are continuously exposed to reactive oxygen species generated by oxidative metabolism, and in certain pathological conditions defense mechanisms against oxygen radicals may be weakened and/or overwhelmed. DNA is a potential target for oxidative damage, and genomic damage can contribute to neuropathogenesis. It is important therefore to identify tools for the quantitative analysis of DNA damage in models on neurological disorders. This book presents detailed information on various neurodegenerative disorders and their connection with oxidative stress. This information will provide clinicians with directions to treat these disorders with appropriate therapy and is also of vital importance for the drug industries for the design of new drugs for treatment of degenerative disorders. * Contains the latest information on the subject of neurodegenerative disorders * Reflects on various factors involved in degeneration and gives suggestions for how to tackle these problems

This book reviews the functions and roles of DJ-1 in various oxidative stress-related diseases and applications of DJ-1 and its binding compounds to the diseases. The DJ-1 gene was first found to be a novel oncogene in 1997 and later, in 2003, also found to be a causative gene for a familial form of Parkinson’s disease (PD), park7. The DJ-1 gene is therefore the first gene discovered that is known to cause cancer and neurodenegerative diseases, including PD. The research field has expanded as the research has developed. Thus this volume begins with a general introduction of DJ-1, and explains the history and research development to understand the following chapters. Those chapters present the roles of DJ-1 in various oxidative stress-related diseases such as neurodegenerative diseases, as well as cancer, diabetes, and fertility. Moreover, several chapters present evidence that DJ-1 is useful for therapeutic strategies against these diseases. The reader will discover that DJ-1 is a promising protein both for basic cell biology and for the mechanism and therapy for oxidative stress-related diseases.

This book examines current knowledge and recent advances in the study of fundamental processes involved in neuronal death, particularly oxidative stress as a causal agent or risk factor. The author presents discussion of oxidative stress in neuronal apoptosis and its role in the neuropathogenesis of age-related neurodegenerative diseases exemplified by Alzheimer's disease, Parkinson's disease and Amyotrophic Lateral Sclerosis.