Sanberg, P (University of South Florida College of Medicine, Tampa Usa)

Mitochondrial Inhibitors and Neurodegenerative Disorders - Contemporary Neuroscience Sanberg, P (University of South Florida College of Medicine, Tampa Usa) 2000 edition

Marc Notes: Includes bibliographical references and index. Review Quotes: ..."is a concise summary of the present state of research in the area of mitochondrial toxins and their role in animal models of neurodegenerative disease."-J Neuropsychiatry Clin NeurosciReview Quotes: .,."is a concise summary of the present state of research in the area of mitochondrial toxins and their role in animal models of neurodegenerative disease."-J Neuropsychiatry Clin NeurosciJacket Description/Back: In Mitochondrial Inhibitors and Neurodegenerative Disorders, respected investigators from around the world critically review what is known about the role of mitochondrial inhibitors in cell death and the onset of neurodegeneration. These distinguished researchers-many pioneers in the field-detail the symptomatology, origin, and chemistry of mitochondrial toxins, and discuss animal models of human diseases related to abnormal mitochondrial function. The book focuses on 3-nitropropionic acid (3-NP) and its ability to replicate the cellular, anatomical, and behavioral alterations seen in Huntington's disease, and demonstrates that mitochondrial inhibitors play an important role in the etiology of central nervous system disorders. In addition, recent therapeutic modalities aimed at rescuing the central nervous system from abnormal functioning by mitochondria are discussed. With its timely, in-depth review, Mitochondrial Inhibitors and Neurodegenerative Disorders offers today's advanced investigators powerful insights into how mitochondrial toxins precipitate and exacerbate neurodegenerative disorders, and details important new treatment strategies that can halt or reverse disease progression. Review Quotes: ."..is a concise summary of the present state of research in the area of mitochondrial toxins and their role in animal models of neurodegenerative disease."-J Neuropsychiatry Clin NeurosciTable of Contents: Part I. Mitochondrial Toxins: Symptomatology, Origin, and Chemistry. Clinical Manifestations and Mechanisms of Action of Environmental Mitochondrial Toxins, Mohammad I. Sabri, Peter S. Spencer, Safia Baggia, and Albert C. Ludolph. History of 3-Nitropropionic Acid: Occurrence and Role in Human and Animal Disease, Bradley F. Hamilton, Daniel H. Gould, and David L. Gustine. The Neurochemistry of 3-Nitropropionic Acid, Norman C. Reynolds, Jr. and Wen Lin. Part II. Mitochondrial Dysfunctions: Models of Neurodegeneration and Mechanisms of Action. In Vitro Studies of 3-Nitropropionic Acid, Gail D. Zeevalk. Cognitive and Motor Deficits Produced by Acute and Chronic Administration of 3-Nitropropionic Acid in Rats, Gary L. Dunbar, Deborah A. Shear, Jie Dong, and Kristi L. Haik-Creguer. Comparative Study on 3-Nitropropionic Acid Neurotoxicity, Cesario V. Borlongan. Mechanisms of 3-Nitropropionic Acid Neurotoxicity, James W. Geddes, Vimala Bondada, and Zhen Pang. Gender-Related Difference of the Effect of 3-Nitropropionic Acid on Striatal Artery, Keiya Nakajima, Yasunobu Shimano, Kunio Torii, and Hitoo Nishino. Variable Susceptibility to Neurotoxicity of Systemic 3-Nitropropionic Acid, Tajrena Alexi, Richard L. M. Faull, and Paul E. Hughes. The 3-Nitropropionic Acid Model of Huntington's Disease: Do Alterations in the Expression of Metabolic mRNAs Predict the Development of Striatal Pathology? Keith J. Page, Alicia Meldrum, and Stephen B. Dunnett. Mechanisms of Action of 3-Nitropropionic Acid: Dopamine Overflow and Vulnerability of the Lateral Striatal Artery, Michiko Kumazaki, Chucharin Ungsuparkorn, Shripad B. Deshpande, Atsuo Fukuda, and Hitoo Nishino. Mitochondrial Inhibition and Neuronal Death in Huntington's Disease, Maria Isabel Behrens. Effects of Brain Mitochondrial Metabolism, Aging, and Caloric Restriction on Membrance Lipids and Proteins: An Electron Paramagnetic Resonance Investigation, S. Prasad Gabbita, John M. Carney, and D. Allan Butterfield. Malonate: Profileand Mechanisms of Striatal Toxicity, Alicia Meldrum, Keith J. Page, Barry J. Everitt, and Stephen B. Dunnett. Malonic Acid and the Chronic Administration Model of Excitotoxicity, Terence J. Bazzett, Roger L. Albin, and Jill B. Becker. Sodium Azide-Induced Neurotoxicity, Yun Wang and Cesario V. Borlongan. Part III. Treatment Interventions for Mitochondrial-Induced Neurotoxicity. Neuroprotective Strategies Against Cellular Hypoxia, Matthias W. Riepe. Neuroprotective Effect of Perinatal Hypoxia Against 3-Nitropropionic Acid Neurotoxicity, Zbigniew K. Binienda and Andrew C. Scallet. Neural Transplantation and Huntington's Disease: What Can We Learn from the 3-Nitropropionic Acid Model? Cesario V. Borlongan, Christine E. Stahl, Thomas B. Freeman, Robert A. Hauser, and Paul R. Sanberg. Neuroprotective Strategies in Parkinson's Disease and Huntington's Chorea: MPTP- and 3-NPA-Induced Neurodegeneration as Models, Moussa B. H. Youdim, Gopal Krishna, and Chuang C. Chiueh. Index."Publisher Marketing: This volume looks at work on the utilization of mitochondrial inhibitors towards understanding the different mechanisms involved in neurodegenerative disorders. The first chapters focus largely on the discovery of environmental mitochondrial dysfunction, but the short historical background provided will help the novice relate basic neurochemistry to mitochondrial dysfunction. Section two deals with the development of animal models of human diseases that are possibly underlied by abnormal mitochondrial functioning, such as Huntington's disease, and studies on the neurotoxin 3-nitropropionic acid (3-NP) are presented by the contributors. The book's concentration is this information on 3-NP, which testifies that mitochondrial inhibitors, in general, play an important role in the aetiology of central nervous system disorders. It concludes with a discussion of the development of treatment strategies and recent therapeutic modalities which are directed towards freeing the central nervous system from abnormal mitochondrial functioning.