Mitochondrial Mechanisms of Degeneration and Repair in Parkinson's Disease (Registro nro. 225567)

MARC details
000 -LIDER
fixed length control field 04420nam a22004695i 4500
001 - CONTROL NUMBER
control field 978-3-319-42139-1
003 - CONTROL NUMBER IDENTIFIER
control field DE-He213
005 - DATE AND TIME OF LATEST TRANSACTION
control field 20180206182938.0
007 - PHYSICAL DESCRIPTION FIXED FIELD--GENERAL INFORMATION
fixed length control field cr nn 008mamaa
008 - FIXED-LENGTH DATA ELEMENTS--GENERAL INFORMATION
fixed length control field 160913s2016 gw | s |||| 0|eng d
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
International Standard Book Number 9783319421391
-- 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 -
-- Cham :
-- Springer International Publishing :
-- Imprint: Springer,
-- 2016.
300 ## - PHYSICAL DESCRIPTION
Extent XII, 275 p. 28 illus., 23 illus. in color.
Other physical details online resource.
336 ## -
-- text
-- txt
-- rdacontent
337 ## -
-- computer
-- c
-- rdamedia
338 ## -
-- online resource
-- cr
-- rdacarrier
347 ## -
-- text file
-- PDF
-- 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 ## -
-- ZDB-2-SBL
942 ## - ADDED ENTRY ELEMENTS (KOHA)
Koha item type Libro Electrónico
Existencias
Estado de retiro Colección Ubicación permanente Ubicación actual Fecha de ingreso Total Checkouts Date last seen Número de copia Tipo de material
  Colección de Libros Electrónicos Biblioteca Electrónica Biblioteca Electrónica 06/02/2018   06/02/2018 1 Libro Electrónico

Con tecnología Koha