Mitochondria And Free Radicals In Neurodegenerative Diseases

The discovery that several major human neurodegenerative diseases are associated with mitochondrial dysfunction has provided new opportunities for a better understanding of these diseases. In this book, major figures in the field offer state-of-the-art reviews of the role of mitochondrial dysfunction and oxidative damage in the pathogenesis of neurodegenerative diseases. Because many of the topics presented overlap with one another, the result is the most comprehensive review of the subject to date. Mitochondria and Free Radicals in Neurodegenerative Diseases begins with a historical overview of the field presented by one of its distinguished founders. The book goes on to supply detailed information on energy metabolism in normal brain function and to explore the role of oxidative damage—which may be a consequence of mitochondrial dysfunction—in the nervous system. Other early chapters focus on energy dysfunction leading to excitotoxic cell damage, the role of mitochondrial toxins in the pathogenesis of animal models of neurodegenerative diseases, and the role of mitochondria in aging. Additional topics include: Neurologic and neuropathologic consequences of mitochondrial disorders The role of mitochondria and oxidative damage in amyotrophic lateral sclerosis, Parkinson's disease, Huntington's disease, Alzheimer's disease, and cerebellar degenerations Using MRI spectroscopy to assess energy defects in patients with neurodegenerative diseases Potential therapies for neurodegenerative diseases The role of glutamate receptor antagonists for therapy Known approaches to improving energy function in mitochondrial disorders Free radical scavengers and other innovative therapeutic approaches Cover image: Three-dimensional reconstruction of an isolated, condensed rat-liver mitochondrion, obtained by electron tomography, courtesy of Dr. Carmen A. Mannella and Wadsworth Center. Reproduced with permission from TiBS (1997) vol. 22, issue 2, pp. 37-38.

Oxidative Stress and Age-Related Neurodegeneration brings together researchers from a variety of fields to compare normal aging and disease-related neurodegeneration in terms of susceptibility to and effects of oxidative stress. They address how these effects can be attenuated, and examine whether antioxidants and natural micronutrients, such as those found in Gingko biloba, green tea, blueberries, and grape seed extract, can play a role. The book includes various ways research is getting to the core of neurodegenerative disease, including the use of proteomics, comparisons to related diseases, and examinations at the cellular and molecular levels.

This book is about the role of both defects in oxidative phosphorylation and oxidative stress in the pathogenesis of neurodegenerative diseases. It describes the relationship between impaired energy metabolism, excytotoxicity and the generation of free radicals. The role of mitochondrial dysfunction in normal aging, and its potential role in the delayed onset of neurodegenerative diseases as well as the result of animal studies using mitochondrial toxins such as MPTP and 3-nitropropionic acid are described. The evidence for both dysfunction and oxidative stress in Alzheimer's disease, Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis are critically reviewed. Lastly, five different therapeutic approaches to treatment of neurodegenerative diseases are discussed.

Mitochondria have long been the Rodney Dangerfield of cellular organelles. Believed to be the remnants of bacterial infection of eukaryotic cells eons ago, the mitochondrion evolved a symbiotic relationship in which it dutifully served as the efficient source of A TP for cell function. The extraordinary dependence of cells on the energy provided by mito chondrial oxidative metabolism of glucose, especially through critical organs such as the heart and brain, is underlined by the fatal consequences of toxins that interfere with the mitochondrial electron transport system. Consistent with their ancestry, the mitochondria have their own DNA that encodes many but not all of their proteins. The mitochon dria and their genes come from the mother via the ovum since sperm do not possess mitochondria. This extranuclear form of inheritance derived exclusively from the female side has proven to be a powerful tool for tracing the evolution by the number of base substitutions in mtDNA. That mitochondrial gene mutations might be a source of human dis ease became evident a decade ago with the characterization of a group of multisystem disorders, typically involving the nervous system, which are transmitted from mother to child. Specific point mutations in mtDNA have been associated with the different syndromes.

This second edition brings together up-to-date contributions from leaders in the field internationally on the various ways in which mitochondrial dysfunction contributes to the pathogenesis of neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease and multiple sclerosis. The reader is guided through the basic functions of mitochondria and the mechanisms that lead to their dysfunction, and on to the consequences of this dysfunction for neuronal function before finishing with the modelling of these disorders and discussion of new potential therapeutic targets. Additional chapters have been added to the book to reflect advances in the field and there are many new contributors and topics, including how mitochondria are degraded and the interaction of the mitochondria with pathologically relevant proteins. Mitochondrial Dysfunction in Neurodegenerative Disorders provides an accessible, authoritative guide to this important area for neurologists; research and clinical neuroscientists; neuropathologists; and residents with an interest in clinical research.

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

The role of oxidative stress in human disease has become an area of intense interest. Free radicals, a normal product of metabolism, exist in all aerobic cells in balance with biochemical antioxidants. Environmental stress increases the levels of free radicals drastically, thereby disturbing the equilibrium between free radical production and the antioxidant capability causing oxidative stress. Over the years, ROS has been implicated in the pathologies of various diseases like cancer, neurological disorder, cardiovascular diseases rheumatoid arthritis, diabetes etc. This book provides an in depth critical state-of-art reviews from established investigators on free radicals, ROS associated pathogenesis of human diseases, biomarkers of oxidative damage, antioxidants, phytonutrients and other related health concerns of modern society. The present book is aimed at graduate students, researchers in academia, industry and clinicians with the interest in redox biology. Special attention has been devoted to the topic of ROS signalling, oxidative stress induced human pathologies & antioxidative therapies. The book consists of four parts in specified topics based on the current literatures for the better understanding of the readers with respect to their subject-wise interests. The first section of the book provides an overview about the ROS production and their measuring tools and techniques followed by the mechanisms involved in the oxidative stress in the second section. The third section describes the involvement of oxidative stress in different human diseases and the last section focuses on the different strategies to ameliorate oxidative stress induced stress.

This volume provides an authoritative, comprehensive view of the most current issues in brain pathophysiology and offers a critical evaluation of antioxidant-based therapeutic approaches to neurodegeneration, providing an up-to-date account of the role of antioxidants in the prevention and moderation of clinical symptoms. Examines free radicals