Mitochondrial Mechanisms of Degeneration and Repair in Parkinson's Disease
This volume brings together various theories of how aberrations in mitochondrial function and morphology contribute to neurodegeneration in idiopathic and familial forms of Parkinson’s disease. Moreover, it comprehensively reviews the current search for t
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Mitochondrial Mechanisms of Degeneration and Repair in Parkinson's Disease
Mitochondrial Mechanisms of Degeneration and Repair in Parkinson’s Disease
Lori M. Buhlman Editor
Mitochondrial Mechanisms of Degeneration and Repair in Parkinson’s Disease
Editor Lori M. Buhlman College of Health Sciences Midwestern University Glendale, AZ, USA
ISBN 978-3-319-42137-7 ISBN 978-3-319-42139-1 DOI 10.1007/978-3-319-42139-1
(eBook)
Library of Congress Control Number: 2016950193 © Springer International Publishing Switzerland 2016 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made. Printed on acid-free paper This Springer imprint is published by Springer Nature The registered company is Springer International Publishing AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland
Preface
Our first close-up views of mitochondria, achieved using transmission electron microscopy, revealed their intracellular distribution and organized double-membrane structure. We know now that fixation techniques used to capture these snapshots deceived us into thinking that these “powerhouses of the cell” existed as a static collection of kidney bean-shaped organelles. Modern technology has revealed that, in fact, mitochondria comprise a highly dynamic network in which sections can break off, move rapidly throughout the cell to deliver energy and calcium-buffering capabilities, and then rejoin the network or be digested in lysosomes. We have learned that mitochondria may have evolved from invasive bacteria to become the most important sensors of cell stress and the gatekeepers of apoptosis. Because most cells rely so heavily on mitochondrial ATP production, and because mitochondrial stress can initiate apoptosis, many deadly diseases are known or thought to be caused by aberrant mitochondrial function. Parkinsonism, which is characterized by the presence of particular motor symptoms caused by degeneration of a subset of dopaminergic neurons in the midbrain, can be induced in animal
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