Studies on Alzheimer's Disease PDF
Preview Studies on Alzheimer's Disease
Oxidative Stress in Applied Basic Research and Clinical Practice Domenico Praticò Patrizia Mecocci Editors Studies on Alzheimer's Disease Oxidative Stress in Applied Basic Research and Clinical Practice Editor-in-Chief Donald Armstrong For further volumes: http://www.springer.com/series/8145 Note from the Editor-in-Chief All books in this series illustrate point-of-care testing and critically evaluate the potential of antioxidant supplementation in various medical disorders associated with oxidative stress. Future volumes will be updated as warranted by emerging new technology, or from studies reporting clinical trials. Donald Armstrong Editor-in-Chief Domenico Praticò (cid:129) Patrizia Mecocci Editors Studies on Alzheimer’s Disease Editors Domenico Praticò Patrizia Mecocci Department of Pharmacology Department of Clinical and Experimental Center for Translational Medicine Medicine Temple University School of Medicine Institute of Gerontology and Geriatrics Philadelphia , PA , USA Ospedale S. Maria della Misericordia Perugia University of Perugia, Perugia , Italy ISBN 978-1-62703-597-2 ISBN 978-1-62703-598-9 (eBook) DOI 10.1007/978-1-62703-598-9 Springer New York Heidelberg Dordrecht London Library of Congress Control Number: 2013947168 © Springer Science+Business Media New York 2013 This work is subject to copyright. 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Printed on acid-free paper Humana Press is a brand of Springer Springer is part of Springer Science+Business Media (www.springer.com) Pref ace Alzheimer’s disease (AD) has no racial, socioeconomic, or geographic boundaries, since it is the most common cause of dementia in elderly individuals throughout the world. As people worldwide live to an older age, AD has become a serious ever-grow- ing public health problem. The importance and the scientifi c challenges of this dis- ease have been well recognized by the neuroscience research community. Approximately 5 % of AD is caused by missense mutations in the gene for either the amyloid β precursor protein (APP) or some of the enzymes (i.e., presenilin-1) involved in its metabolism. However, in its sporadic form, which is the most fre- quent, the cause(s) remains unknown. Among different potential mechanisms, the combination of genetic risk factors with abnormal metabolic oxidative reactions in the central nervous system has been consistently implicated in the pathogenesis of the disease, and represents the bio- logical basis for the “oxidative stress hypothesis of AD” which was originally for- mulated by Markesbery in his article of 1997. Since then, many studies, ranging from basic research to clinical and epidemio- logical observations, strongly support what moved from a hypothesis to a certainty: the core role of the slight unbalance between oxidants and antioxidants (redox sta- tus) that represents an input for life and, in the meantime, a risk for dysfunction and disease when uncontrolled (oxidative stress). So, after several years from its pro- posal, it seems appropriate to look and consider all the remarkable advances achieved in understanding the biological complexity and mechanistic relationship between oxidative stress and AD. In constructing this book, we have tried to draw upon our own experiences and those of our colleagues in order to present the current status of both basic and clini- cal science research in this specifi c area. The authors are expert scientists who are directly involved in the laboratory and clinical research in the fi eld of oxidative metabolism and neurodegenerative dis- eases with special focus on AD. The book is divided into three main sections. The fi rst section focuses on new working hypotheses implicating oxidative stress and AD. Its chapters will provide v vi Preface the reader with insights into the impact that the oxidative stress hypothesis had in neuroscience research (Chap. 1 ), an overview on the general phenomenon of oxida- tive stress (Chap. 2 ), its intricate connection with infl ammation (Chap. 3 ), new experimental evidence involving an old enzyme such as GADPH (Chap. 4 ), the relationship between mitochondria and Aβ (Chap. 5 ), and the new role that plasma membrane plays in controlling the cellular redox system (Chap. 6 ). The second section reviews some of the cellular and metabolic oxidative mecha- nisms that have been involved in AD pathogenesis. After focusing on metal dysho- meostasis (Chap. 7 ) and oxidative posttranslational modifi cation of proteins (Chap. 8 ), it continues with the analysis of cholesterol oxidative metabolism (Chap. 9 ), and the provocative theme of brain hypometabolism, oxidative stress, and maternal transmis- sion of AD (Chap. 1 0 ), fi nishing with the role on HPA dysfunction and AD (Chap. 1 1 ). The third section describes the clinical aspects and implications of the oxidative stress hypothesis in the AD neurobiology. In these fi nal chapters the attention is shifted towards the translational aspects of the oxidative stress hypothesis, with the main goal to apply the knowledge accumulated so far into a clinical scenario by looking at preventative as well as therapeutic opportunities derived from it. The role that diabetes plays in AD pathophysiology will be considered (Chap. 12 ), and the clinical topics will expand on the current state of the art on peripheral biological measure of oxidative stress in AD (Chap. 1 3 ). These two chapters will be followed by the analysis of modifi able environmental risk factors such as nutrition and lifestyle and the risk of AD (Chap. 1 4 ), and the intriguing question of the use- fulness of nutrients as an important source for antioxidants in preventing cognitive decline (Chap. 1 5 ). This section will conclude our editorial effort with an analytical review of the clinical trials that have used antioxidants in mild cognitive impair- ments and AD (Chap. 1 6 ). No introduction would be complete without a grateful acknowledgement of many friends and colleagues who did the work and wrote the chapters. They are not just experts in their fi elds but also extraordinary individuals. Thus, without any shadow of doubt this endeavor was enabled by the contributions of many friends, collaborators, and colleagues, without whose enthusiasm and engagement this work could have never been born. An extraordinary link of science and friendship that was really supportive in constructing this book. While we largely underestimated the devotion and effort necessary on our side at the beginning, we strongly believe that it ultimately yielded an excellent product which fully achieves our original plans. Despite the fact that we confront a continu- ously evolving topic, where frequent updates would be desirable, if not necessary, we believe in the value of a book like ours that attempts to organize in a snapshot- picture type of work, the enormous amount of literature available in a comprehen- sive and fulfi lling fashion. We are aware of possible gaps, some emerging materials not included, and the ever-rapid evolution of some of the themes highlighted in the book. It is our hope that our colleagues, neurobiologists, neurologists, internists, geriatricians, and other physicians alike will fi nd this compendium a useful guide to this most exciting time in the neurobiology of AD. Philadelphia, PA, USA Domenico Praticò Perugia, Italy Patrizia Mecocci Contents Part I Hypotheses 1 Oxidative Stress: Impact in Neuroscience Research ............................ 3 Helmut Sies 2 Oxidative Stress and Alzheimer’s Disease ............................................ 9 Rudy J. Castellani, Bei-Xu Li, Amna Farshori, and Georgy Perry 3 Infl ammation and Oxidation: A Link in Alzheimer’s Disease Pathogenesis ............................................................................... 15 Kenneth Hensley 4 GAPDH: β-Amyloid Mediated Iron Accumulation in Alzheimer’s Disease: A New Paradigm for Oxidative Stress Induction in Neurodegenerative Disorders ............................... 25 Michael A. Sirover 5 Aβ in Mitochondria—One Piece in the Alzheimer’s Disease Puzzle .......................................................................................... 41 Maria Ankarcrona 6 The Role of the Plasma Membrane Redox System in the Pathogenesis of Alzheimer’s Disease........................................... 55 Sara M. Hancock, David I. Finkelstein, Ashley I. Bush, and Paul A. Adlard Part II Mechanisms 7 Metal Dysfunction in Alzheimer’s Disease............................................ 73 Rosanna Squitti, Mariacristina Siotto, Carlo Salustri, and Renato Polimanti vii viii Contents 8 Brain Oxidative Stress in the Pathogenesis and Progression of Alzheimer’s Disease ................................................ 99 Rukhsana Sultana, Aaron M. Swomley, and D. Allan Butterfi eld 9 Cholesterol Metabolism and Oxidative Stress in Alzheimer’s Disease ............................................................................ 119 Luigi Iuliano and Valerio Leoni 10 Brain Hypometabolism, Oxidative Stress, Maternal Transmission, and Risk of Late-Onset Alzheimer’s Disease ........................................ 137 Lisa Mosconi, John Murray, Pauline McHugh, and Mony de Leon 11 Stress and HPA Axis Dysfunction in Alzheimer’s Disease ................... 159 Yash B. Joshi and Domenico Praticò Part III Clinics 12 Diabetes Mellitus and Its Impact on Sporadic Alzheimer’s Disease .................................................................................. 169 Weili Xu 13 Peripheral Biomarkers of Oxidative Stress in Alzheimer’s Disease ............................................................................. 185 Fabio Di Domenico and Marzia Perluigi 14 Nutrition, Lifestyle and Oxidative Stress: Prevention of Alzheimer’s Disease ......................................................... 201 M. Cristina Polidori and Ludger Pientka 15 Are Antioxidant Food and Nutrients Useful in Preventing Cognitive Decline? .................................................................................. 211 Luc Letenneur, Catherine Feart, and Pascale Barberger-Gateau 16 Antioxidant Clinical Trials in Mild Cognitive Impairment and Alzheimer’s Disease ......................................................................... 223 Patrizia Mecocci, M. Cristina Polidori, and Domenico Praticó About the Editors ............................................................................................ 233 Index ................................................................................................................. 235 Contributors Paul A. Adlard, Ph.D. Synaptic Neurobiology Laboratory, The Florey Institute of Neuroscience and Mental Health , Parkville , VIC , Australia Maria Ankarcrona, Ph.D. Department of Neurobiology, Care Sciences and Society, KI-Alzheimer’s Disease Center (KI-ADCR) , Karolinska Institutet , Stockholm , Sweden Pascale Barberger-Gateau, Ph.D. ISPED, Centre INSERM U897 – Epidemiologie-Biostatistique , University of Bordeaux , Bordeaux , France INSERM, ISPED, Centre INSERM U897–Epidemiologie-Biostatistique, Bordeaux, France Ashley I. Bush, Ph.D. Oxidation Biology Laboratory, The Florey Institute of Neuroscience and Mental Health , Parkville , VIC , Australia D. Allan Butterfi eld, Ph.D. Department of Chemistry, Center of Membrane Sciences, The Sanders-Brown Center on Aging , University of Kentucky , Lexington , KY , USA Rudy J. Castellani, Ph.D. Division of Neuropathology, Department of Pathology , University of Maryland , Baltimore , MD , USA Fabio Di Domenico, Ph.D. Department of Biochemical Sciences , Sapienza University of Rome , Rome , Italy Amna Farshori, Ph.D. Department of Pathology , University of Maryland , Baltimore , MD , USA Catherine Feart, Ph.D. ISPED, Centre INSERM U897 – Epidemiologie- Biostatistique , University of Bordeaux , Bordeaux , France INSERM, ISPED, Centre INSERM U897 – Epidemiologie-Biostatistique , B ordeaux , France ix
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