Mitochondrial Mechanisms of Degeneration and Repair in Parkinson's Disease

Nonfiction, Health & Well Being, Medical, Specialties, Internal Medicine, Neuroscience, Science & Nature, Science, Biological Sciences, Zoology
Cover of the book Mitochondrial Mechanisms of Degeneration and Repair in Parkinson's Disease by , Springer International Publishing
View on Amazon View on AbeBooks View on Kobo View on B.Depository View on eBay View on Walmart
Author: ISBN: 9783319421391
Publisher: Springer International Publishing Publication: September 13, 2016
Imprint: Springer Language: English
Author:
ISBN: 9783319421391
Publisher: Springer International Publishing
Publication: September 13, 2016
Imprint: Springer
Language: English

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.

View on Amazon View on AbeBooks View on Kobo View on B.Depository View on eBay View on Walmart

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.

More books from Springer International Publishing

Cover of the book Cellular Therapies for Retinal Disease by
Cover of the book New Approaches to Death in Cities during the Health Transition by
Cover of the book High Dimensional Probability VII by
Cover of the book The Quantum Gamble by
Cover of the book Grand Challenges in Technology Enhanced Learning by
Cover of the book Silicon Light-Emitting Diodes and Lasers by
Cover of the book Real-Time Recursive Hyperspectral Sample and Band Processing by
Cover of the book Ocular Drug Delivery: Advances, Challenges and Applications by
Cover of the book Explicit and Implicit Prosody in Sentence Processing by
Cover of the book Multispectral Biometrics by
Cover of the book Natural Gas Seepage by
Cover of the book Dissecting Regulatory Interactions of RNA and Protein by
Cover of the book Probability and Statistics for Particle Physics by
Cover of the book The Responsibilities of Online Service Providers by
Cover of the book Pediatric Endocrinology by
We use our own "cookies" and third party cookies to improve services and to see statistical information. By using this website, you agree to our Privacy Policy