© 2016

Mitochondrial Mechanisms of Degeneration and Repair in Parkinson's Disease

  • Lori M. Buhlman


  • Summarizes theories of how poor mitochondrial function and morphology contribute to neurodegeneration

  • Discusses both sporadic and familial forms of Parkinson's disease

  • Proposes potential molecules that would make attractive therapeutic targets


Table of contents

  1. Front Matter
    Pages i-xii
  2. Hazem El-Osta, Magdalena L. Circu
    Pages 1-23
  3. Sylvie Delcambre, Yannic Nonnenmacher, Karsten Hiller
    Pages 25-47
  4. Li Zuo, Tingyang Zhou, Chia-Chen Chuang
    Pages 49-61
  5. Velmarini Vasquez, Joy Mitra, Erika N. Guerrero, Pavana M. Hegde, K. S. Rao, Muralidhar L. Hegde
    Pages 75-113
  6. Briana R. De Miranda, Bennett Van Houten, Laurie H. Sanders
    Pages 115-137
  7. Javier Blesa, Ines Trigo-Damas, Ana Quiroga-Varela, Natalia Lopez-Gonzalez del Rey
    Pages 139-158
  8. Ana Raquel Esteves, Diana F. Silva, Maria G-Fernandes, Rui Gomes, Sandra Morais Cardoso
    Pages 183-205
  9. Diana Guzman-Villanueva, Volkmar Weissig
    Pages 255-267
  10. Back Matter
    Pages 269-275

About this book


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 therapies, and proposes how molecules are involved in specific functions as attractive therapeutic targets. It is expected to facilitate critical thought and discussion about the fundamental aspects of neurodegeneration in Parkinson’s disease and foster the development of therapeutic strategies among researchers and graduate students. Theories of idiopathic Parkinson’s etiology support roles for chronic inflammation and exposure to heavy metals or pesticides. Interestingly, as this project proposes, a case can be made that abnormalities in mitochondrial morphology and function are at the core of each of these theories. In fact, the most common approach to the generation of animal and cell-culture models of idiopathic Parkinson’s disease involves exposure to mitochondrial toxins. Even more compelling is the fact that most familial patients harbor genetic mutations that cause disruptions in normal mitochondrial morphology and function. While there remains to be no effective treatment for Parkinson’s disease, efforts to postpone, prevent and “cure” onset mitochondrial aberrations and neurodegeneration associated with Parkinson’s disease in various models are encouraging. While only about ten percent of Parkinson’s patients inherit disease-causing mutations, discovering common mechanisms by which familial forms of Parkinson’s disease manifest will likely shed light on the pathophysiology of the more common idiopathic form and provide insight to the general process of neurodegeneration, thus revealing therapeutic targets that will become more and more accessible as technology improves.


Drosophila melanogaster Parkinson's Disease dopaminergic neuron mitochondria neurodegeneration reactive oxygen species

Editors and affiliations

  • Lori M. Buhlman
    • 1
  1. 1.College of Health SciencesMidwestern UniversityGlendaleUSA

About the editors

Lori Buhlman earned her Ph.D. in Neuroscience from the University of Arizona and trained as a post-doctoral fellow at the Institut National de la Santé et de la Recherche Médicale, in Paris, France.  She is currently an associate professor of Biomedical Sciences and Behavioral Medicine at Midwestern University in Glendale, Arizona, where she manages a research program exploring the mechanisms by which loss of Parkin function causes neurodegeneration.  Her recent publications report that nicotine can protect against motor deficits caused by Parkin loss of function in Drosophila, and that Parkin and PINK1 work together to promote mitochondrial homeostasis in a manner that involves mitochondrial fission protein, Drp1. 

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