Report file quality
lgli/K:\!genesis\!repository8\sp\10.1007%2F978-3-319-42139-1.pdf
Mitochondrial Mechanisms of Degeneration and Repair in Parkinson's Disease 🔍
Lori M. Buhlman (eds.) Springer International Publishing : Imprint: Springer, 1st ed. 2016, Cham, 2016
English [en] · PDF · 8.0MB · 2016 · 📘 Book (non-fiction) · 🚀/lgli/lgrs/nexusstc/scihub/zlib · Save
description
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.
Erscheinungsdatum: 23.09.2016
Alternative filename
lgrsnf/K:\!genesis\!repository8\sp\10.1007%2F978-3-319-42139-1.pdf
Alternative filename
nexusstc/Mitochondrial Mechanisms of Degeneration and Repair in Parkinson's Disease/127ce143c7b4005c457c59f7041daf43.pdf
Alternative filename
scihub/10.1007/978-3-319-42139-1.pdf
Alternative filename
zlib/Medicine/Lori M. Buhlman (eds.)/Mitochondrial Mechanisms of Degeneration and Repair in Parkinson's Disease_2803544.pdf
Alternative author
Lori M Buhlman; SpringerLink (Online service)
Alternative author
Buhlman, Lori M.
Alternative author
Author
Alternative publisher
Springer Nature Switzerland AG
Alternative publisher
Springer London, Limited
Alternative edition
Springer Nature, Cham, Switzerland, 2016
Alternative edition
Switzerland, Switzerland
Alternative edition
New York, 2016
Alternative edition
Sep 14, 2016
Alternative edition
2, 20160913
Alternative edition
1, 2019
metadata comments
sm61452642
metadata comments
{"edition":"1","isbns":["3319421379","3319421395","9783319421377","9783319421391"],"publisher":"Springer"}
Alternative description
This volume brings together various theories of how aberrations in mitochondrial function and morphology contribute to neurodegeneration in idiopathic and familial forms of Parkinson{u2019}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{u2019}s disease and foster the development of therapeutic strategies among researchers and graduate students. Theories of idiopathic Parkinson{u2019}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{u2019}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{u2019}s disease, efforts to postpone, prevent and 2cure3 onset mitochondrial aberrations and neurodegeneration associated with Parkinson{u2019}s disease in various models are encouraging. While only about ten percent of Parkinson{u2019}s patients inherit disease-causing mutations, discovering common mechanisms by which familial forms of Parkinson{u2019}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
Alternative description
Annotation The firstvolume to bring together various theories of how aberrations in mitochondrial function and morphology contribute to neurodegeneration in idiopathic and familial forms of Parkinson's disease, to comprehensively review the current search for therapies, and to propose molecules 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 biomedical sciences 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 onset, prevent and "cure" 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
Alternative description
Front Matter....Pages i-xii
Mitochondrial ROS and Apoptosis....Pages 1-23
Dopamine Metabolism and Reactive Oxygen Species Production....Pages 25-47
The Consequences of Damaged Mitochondrial DNA....Pages 49-61
The Role of Chronic Inflammation in the Etiology of Parkinson’s Disease....Pages 63-74
Ion-Catalyzed Reactive Oxygen Species in Sporadic Models of Parkinson’s Disease....Pages 75-113
Toxin-Mediated Complex I Inhibition and Parkinson’s Disease....Pages 115-137
Parkinson’s Disease-Associated Mutations Affect Mitochondrial Function....Pages 139-158
PARKIN/PINK1 Pathway for the Selective Isolation and Degradation of Impaired Mitochondria....Pages 159-182
Mitochondrial Therapeutic Approaches in Parkinson’s Disease....Pages 183-205
Altering Mitochondrial Fusion and Fission Protein Levels Rescues Parkin and PINK1 Loss-of-Function Phenotypes....Pages 207-218
Early Nicotine Exposure Is Protective in Familial and Idiopathic Models of Parkinson’s Disease....Pages 219-229
Transcription Modulation of Mitochondrial Function and Related Pathways as a Therapeutic Opportunity in Parkinson’s Disease....Pages 231-253
Delivery of Biologically Active Molecules to Mitochondria....Pages 255-267
Back Matter....Pages 269-275
date open sourced
2016-11-20
Read more…

🚀 Fast downloads

Become a member to support the long-term preservation of books, papers, and more. To show our gratitude for your support, you get fast downloads. ❤️

🐢 Slow downloads

From trusted partners. More information in the FAQ. (might require browser verification — unlimited downloads!)

All download options have the same file, and should be safe to use. That said, always be cautious when downloading files from the internet, especially from sites external to Anna’s Archive. For example, be sure to keep your devices updated.
show external downloads
  • For large files, we recommend using a download manager to prevent interruptions.
    Recommended download managers: Motrix
  • You will need an ebook or PDF reader to open the file, depending on the file format.
    Recommended ebook readers: Anna’s Archive online viewer, ReadEra, and Calibre
  • Use online tools to convert between formats.
    Recommended conversion tools: CloudConvert and PrintFriendly
  • You can send both PDF and EPUB files to your Kindle or Kobo eReader.
    Recommended tools: Amazon‘s “Send to Kindle” and djazz‘s “Send to Kobo/Kindle”
  • Support authors and libraries
    ✍️ If you like this and can afford it, consider buying the original, or supporting the authors directly.
    📚 If this is available at your local library, consider borrowing it for free there.