Fr. 147.00

Oxidative Neural Injury

Englisch · Taschenbuch

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Beschreibung

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Twenty-five years ago, Earl R. Stadtman, PhD discovered that specific enzymes regulating metabolism can be inactivated by oxidation [1]. He later showed that age-related oxidative modification contributes, at least in part, to age-related loss of function of the enzymes [2, 3]. Dr. Stadtman broke the ground for a new field of study to discover how oxidative stress contributes in significant ways to age-related cellular dysfunction and protein accumulation and that oxidation in the aging brain influences Alzheimer's disease, ischemia-reperfusion injury, amyotrophic lateral sclerosis, and lifespan [4-6]. Today, his research and mentorship have positively influenced the work of hundreds of scientists in this field. We dedicate this book to Dr. Earl R. Stadtman (1912-2008), in celebration of his passion for science and his superior collaborative and mentorship skills. This book is comprised of three sections. The first describes the valuable roles reactive oxygen species (ROS) and reactive nitrogen species (RNS) play in cellular biology. The second section provides an overview of redox imbalance injury with effects on mitochondria, signaling, endoplasmic reticular function, and on aging in general. The third section takes these mechanisms to neurodegenerative disorders and provides a state-of-the-art look at the roles redox imbalances play in age-related susceptibility to disease and in the disease processes. In the first section we attempt to answer a question posed by Dr. Stadtman, ''Why have cells selected reactive oxygen species to regulate cell signaling events'' [7].

Inhaltsverzeichnis

Reactive Oxygen Species, Synaptic Plasticity, and Memory.- Nitric Oxide Biochemistry: Pathophysiology of Nitric Oxide-Mediated Protein Modifications.- Redox Imbalance in the Endoplasmic Reticulum.- Exocytosis, Mitochondrial Injury and Oxidative Stress in Neurodegenerative Diseases.- Neuronal Vulnerability to Oxidative Damage in Aging.- Ischemia-Reperfusion Induces ROS Production from Three Distinct Sources.- Alzheimer Disease: Oxidative Stress and Compensatory Responses.- Oxidative Stress Associated Signal Transduction Cascades in Alzheimer Disease.- Nitrated Proteins in the Progression of Alzheimer's Disease: A Proteomics Comparison of Mild Cognitive Impairment and Alzheimer's Disease Brain.- Parkinson's Disease: An Overview of Pathogenesis.- Protein Oxidation Triggers the Unfolded Protein Response and Neuronal Injury in Chemically Induced Parkinson Disease.- Treating Oxidative Neural Injury: Methionine Sulfoxide Reductase Therapy for Parkinson's Disease.

Zusammenfassung

Twenty-five years ago, Earl R. Stadtman, PhD discovered that specific enzymes regulating metabolism can be inactivated by oxidation [1]. He later showed that age-related oxidative modification contributes, at least in part, to age-related loss of function of the enzymes [2, 3]. Dr. Stadtman broke the ground for a new field of study to discover how oxidative stress contributes in significant ways to age-related cellular dysfunction and protein accumulation and that oxidation in the aging brain influences Alzheimer’s disease, ischemia-reperfusion injury, amyotrophic lateral sclerosis, and lifespan [4–6]. Today, his research and mentorship have positively influenced the work of hundreds of scientists in this field. We dedicate this book to Dr. Earl R. Stadtman (1912–2008), in celebration of his passion for science and his superior collaborative and mentorship skills. This book is comprised of three sections. The first describes the valuable roles reactive oxygen species (ROS) and reactive nitrogen species (RNS) play in cellular biology. The second section provides an overview of redox imbalance injury with effects on mitochondria, signaling, endoplasmic reticular function, and on aging in general. The third section takes these mechanisms to neurodegenerative disorders and provides a state-of-the-art look at the roles redox imbalances play in age-related susceptibility to disease and in the disease processes. In the first section we attempt to answer a question posed by Dr. Stadtman, ‘‘Why have cells selected reactive oxygen species to regulate cell signaling events’’ [7].

Zusatztext

From the reviews:

“This book addresses how oxidative stress contributes to age-related cellular dysfunction particularly in Alzheimer's ischemia, Parkinson's disease, and other neurodegenerative conditions. The book fills a niche, addressing the current molecular understanding of oxidative stress and its role in pathophysiology. … it is most appropriate for the many neuroscientists around the world contemplating how to identify the next best approach for targeted therapy for several neurodegenerative diseases. … the book is a good resource for libraries with PhD graduate students and molecular neuroscience laboratories.” (Joseph I. Sirven, Doody’s Review Service, December, 2009)

Bericht

From the reviews: "This book addresses how oxidative stress contributes to age-related cellular dysfunction particularly in Alzheimer's ischemia, Parkinson's disease, and other neurodegenerative conditions. The book fills a niche, addressing the current molecular understanding of oxidative stress and its role in pathophysiology. ... it is most appropriate for the many neuroscientists around the world contemplating how to identify the next best approach for targeted therapy for several neurodegenerative diseases. ... the book is a good resource for libraries with PhD graduate students and molecular neuroscience laboratories." (Joseph I. Sirven, Doody's Review Service, December, 2009)

Produktdetails

Mitarbeit Sigri C Veasey (Herausgeber), Sigrid C Veasey (Herausgeber), Sigrid C. Veasey (Herausgeber)
Verlag Springer, Berlin
 
Sprache Englisch
Produktform Taschenbuch
Erschienen 26.07.2011
 
EAN 9781617378928
ISBN 978-1-61737-892-8
Seiten 218
Gewicht 355 g
Illustration XIV, 218 p. 16 illus.
Serien Contemporary Clinical Neuroscience
Contemporary Clinical Neurosci
Contemporary Clinical Neuroscience
Contemporary Clinical Neurosci
Themen Naturwissenschaften, Medizin, Informatik, Technik > Medizin > Klinische Fächer

Physiologie, Biochemie, C, Neurowissenschaften, Neurology, HUMAN PHYSIOLOGY, PHYSIOLOGY, Neuroscience, biochemistry, Neurosciences, Biomedical and Life Sciences, Biochemistry, general, Neurobiology

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