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Non-fibrillar Amyloidogenic Protein Assemblies - Common Cytotoxins Underlying Degenerative Diseases (Record no. 18741)

000 -LEADER
fixed length control field 04619nam a22004935i 4500
003 - CONTROL NUMBER IDENTIFIER
control field OSt
005 - DATE AND TIME OF LATEST TRANSACTION
control field 20140310150251.0
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 120110s2012 ne | s |||| 0|eng d
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
International Standard Book Number 9789400727748
978-94-007-2774-8
050 #4 - LIBRARY OF CONGRESS CALL NUMBER
Classification number R-RZ
082 04 - DEWEY DECIMAL CLASSIFICATION NUMBER
Classification number 610
Edition number 23
264 #1 -
-- Dordrecht :
-- Springer Netherlands,
-- 2012.
912 ## -
-- ZDB-2-SBL
100 1# - MAIN ENTRY--PERSONAL NAME
Personal name Rahimi, Farid.
Relator term editor.
245 10 - IMMEDIATE SOURCE OF ACQUISITION NOTE
Title Non-fibrillar Amyloidogenic Protein Assemblies - Common Cytotoxins Underlying Degenerative Diseases
Medium [electronic resource] /
Statement of responsibility, etc edited by Farid Rahimi, Gal Bitan.
300 ## - PHYSICAL DESCRIPTION
Extent VIII, 568 p.
Other physical details online resource.
505 0# - FORMATTED CONTENTS NOTE
Formatted contents note 1. Overview of Fibrillar and Oligomeric Assemblies of Amyloidogenic Proteins -- 2. Pathologic Lesions in Alzheimer disease and Other Neurodegenerative Diseases—Cellular and Molecular Components -- 3. Preparation and Structural Characterization of Pre-fibrillar Assemblies of Amyloidogenic Proteins -- 4. Biological Targeting and Activity of Pre-fibrillar Aβ Assemblies -- 5. The Role of Aβ and Tau Oligomers in the Pathogenesis of Alzheimer’s disease -- 6. Oligomers of α-Synuclein in the Pathogenesis of Parkinson’s Disease -- 7. Cytotoxic Mechanisms of Islet Amyloid Polypeptide in the Pathogenesis of Type-2 Diabetes Mellitus (T2DM) -- 8. Protein Misfolding and Toxicity in Amyotrophic Lateral Sclerosis -- 9. Structural Studies of Prion Proteins and Prions -- 10. Role of Prion Protein Oligomers in the Pathogenesis of Transmissible Spongiform Encephalopathies -- 11. When More Is Not Better: Expanded Polyglutamine Domains in Neurodegenerative Disease -- 12. Protein Misfolding and Toxicity in Dialysis-Related Amyloidosis -- 13. Transthyretin Aggregation and Toxicity -- 14. Strategies for Inhibiting Protein Aggregation: Therapeutic Approaches to Protein-Aggregation Diseases.
520 ## - SUMMARY, ETC.
Summary, etc Aberrant protein folding and self-assembly underlie over 30 human diseases called amyloidoses, for which currently there is no cure. The diseases range from tissue-specific to systemic and from genetic to sporadic. Some of the most devastating amyloidoses are those that affect the central nervous system (CNS), such as Alzheimer’s disease (AD), Parkinson’s disease (PD), prionoses (e.g., mad-cow disease), and amyotrophic lateral sclerosis (Lou Gehrig’s disease). In each disease, one or more proteins self-associate into toxic oligomers that disrupt cellular function and communication, and proceed to form insoluble amyloid aggregates characterized by fibrillar morphology and cross-β structure. The first decade of the 21st century has brought with it significant progress in our understanding of amyloid diseases, including the physiological and pathological processes involving each of the offending proteins. Important developments also provide now improved diagnoses of different amyloidoses and new approaches are being developed towards disease-modifying therapies. This book covers the current state-of-the-art knowledge on amyloidoses as a general phenomenon and offers detailed reviews of individual amyloid-forming proteins and specific diseases. Features: Coverage of the pathologic and pathogenic structures of amyloidogenic proteins from the pathological lesions to the evasive oligomers that are believed to be the main culprits. Detailed discussions of diseases of epidemic proportion, such as Alzheimer’s disease, Parkinson’s disease, and type-2 diabetes. Current reviews of multiple diseases, including amyotrophic lateral sclerosis, prionoses, expanded polyglutamine diseases, dialysis-related amyloidosis, and transthyretin-related amyloidoses. Mechanism-based strategies for inhibiting protein aggregation and potential therapeutic applications in different diseases.
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Medicine.
Topical term or geographic name as entry element Neurosciences.
Topical term or geographic name as entry element Pathology.
Topical term or geographic name as entry element Biochemistry.
Topical term or geographic name as entry element Neurobiology.
Topical term or geographic name as entry element Biomedicine.
Topical term or geographic name as entry element Biomedicine general.
Topical term or geographic name as entry element Protein Science.
Topical term or geographic name as entry element Protein Structure.
Topical term or geographic name as entry element Neurosciences.
Topical term or geographic name as entry element Neurobiology.
Topical term or geographic name as entry element Pathology.
700 1# - ADDED ENTRY--PERSONAL NAME
Personal name Bitan, Gal.
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
Display text Printed edition:
International Standard Book Number 9789400727731
856 40 - ELECTRONIC LOCATION AND ACCESS
Uniform Resource Identifier http://dx.doi.org/10.1007/978-94-007-2774-8
942 ## - ADDED ENTRY ELEMENTS (KOHA)
Source of classification or shelving scheme
Item type E-Book
Copies
Price effective from Permanent location Date last seen Not for loan Date acquired Source of classification or shelving scheme Koha item type Damaged status Lost status Withdrawn status Current location Full call number
2014-04-08AUM Main Library2014-04-08 2014-04-08 E-Book   AUM Main Library610

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