MARC details
000 -LIDER |
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04420nam a22004695i 4500 |
001 - CONTROL NUMBER |
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978-3-319-42139-1 |
003 - CONTROL NUMBER IDENTIFIER |
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DE-He213 |
005 - DATE AND TIME OF LATEST TRANSACTION |
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20180206182938.0 |
007 - PHYSICAL DESCRIPTION FIXED FIELD--GENERAL INFORMATION |
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008 - FIXED-LENGTH DATA ELEMENTS--GENERAL INFORMATION |
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160913s2016 gw | s |||| 0|eng d |
020 ## - INTERNATIONAL STANDARD BOOK NUMBER |
International Standard Book Number |
9783319421391 |
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978-3-319-42139-1 |
050 #4 - LIBRARY OF CONGRESS CALL NUMBER |
Classification number |
QP356.3 |
072 #7 - SUBJECT CATEGORY CODE |
Subject category code |
MJN |
Source |
bicssc |
072 #7 - SUBJECT CATEGORY CODE |
Subject category code |
MED057000 |
Source |
bisacsh |
082 04 - DEWEY DECIMAL CLASSIFICATION NUMBER |
Classification number |
612.8042 |
Edition number |
23 |
245 10 - TITLE STATEMENT |
Title |
Mitochondrial Mechanisms of Degeneration and Repair in Parkinson's Disease |
Medium |
[recurso electrónico] / |
Statement of responsibility, etc. |
edited by Lori M. Buhlman. |
264 #1 - |
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Cham : |
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Springer International Publishing : |
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Imprint: Springer, |
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2016. |
300 ## - PHYSICAL DESCRIPTION |
Extent |
XII, 275 p. 28 illus., 23 illus. in color. |
Other physical details |
online resource. |
336 ## - |
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text |
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txt |
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rdacontent |
337 ## - |
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computer |
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rdamedia |
338 ## - |
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online resource |
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cr |
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rdacarrier |
347 ## - |
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text file |
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PDF |
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rda |
505 0# - FORMATTED CONTENTS NOTE |
Formatted contents note |
Mitochondrial ROS and Apoptosis -- Dopamine Metabolism and Reactive Oxygen Species Production -- The Consequences of Damaged Mitochondrial DNA -- The role of chronic inflammation in the etiology of Parkinson?s disease -- Ion-Catalyzed Reactive Oxygen Species in Sporadic Models of Parkinson's Disease -- Toxin Mediated Complex I Inhibition and Parkinson?s Disease -- Parkinson Disease-Associated Mutations Affect Mitochondrial Function -- PARKIN/PINK1 Pathway for the Selective Isolation and Degradation of Impaired Mitochondria -- Mitochondrial Therapeutic approaches in Parkinson's Disease -- Altering Mitochondrial Fusion and Fission Protein Levels Rescues Parkin and PINK1 Loss-of-Function Phenotypes -- Early Nicotine Exposure is Protective in Familial and Idiopathic Models of Parkinson?s Disease -- Transcription Modulation of Mitochondrial Function and Related Pathways as a Therapeutic Opportunity in Parkinson?s Disease -- Delivery of Biologically Active Molecules to Mitochondria. |
520 ## - SUMMARY, ETC. |
Summary, etc. |
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. |
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM |
Término temático o nombre geográfico como elemento de entrada |
Medicine. |
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM |
Término temático o nombre geográfico como elemento de entrada |
Neurochemistry. |
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM |
Término temático o nombre geográfico como elemento de entrada |
Neurology. |
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM |
Término temático o nombre geográfico como elemento de entrada |
Neurobiology. |
650 14 - SUBJECT ADDED ENTRY--TOPICAL TERM |
Término temático o nombre geográfico como elemento de entrada |
Biomedicine. |
650 24 - SUBJECT ADDED ENTRY--TOPICAL TERM |
Término temático o nombre geográfico como elemento de entrada |
Neurochemistry. |
650 24 - SUBJECT ADDED ENTRY--TOPICAL TERM |
Término temático o nombre geográfico como elemento de entrada |
Neurobiology. |
650 24 - SUBJECT ADDED ENTRY--TOPICAL TERM |
Término temático o nombre geográfico como elemento de entrada |
Neurology. |
700 1# - ADDED ENTRY--PERSONAL NAME |
Personal name |
Buhlman, Lori M. |
Relator term |
editor. |
710 2# - ADDED ENTRY--CORPORATE NAME |
Corporate name or jurisdiction name as entry element |
SpringerLink (Online service) |
773 0# - HOST ITEM ENTRY |
Title |
Springer eBooks |
776 08 - ADDITIONAL PHYSICAL FORM ENTRY |
Relationship information |
Printed edition: |
International Standard Book Number |
9783319421377 |
856 40 - ELECTRONIC LOCATION AND ACCESS |
Public note |
Libro electrónico |
Uniform Resource Identifier |
http://148.231.10.114:2048/login?url=http://dx.doi.org/10.1007/978-3-319-42139-1 |
912 ## - |
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ZDB-2-SBL |
942 ## - ADDED ENTRY ELEMENTS (KOHA) |
Koha item type |
Libro Electrónico |