Notch from Neurodevelopment to Neurodegeneration: Keeping the Fate
Published on 28. May 2002
Book
Hardback
XVI, 158 pages
978-3-540-43073-5 (ISBN)
Description
Can molecular mechanisms involved in neural development help us to understand, prevent and perhaps reverse the course of brain ageing and neurodegenerative disorders? Brain development and function require complex cellular and molecular processes controlled by a number of different signaling mechanisms. One such signaling mechanism, the Notch pathway, has been recognized as an important player in the regulation of cellfate decisions during early neural development. However, the action of this evolutionary conserved and widely used cell-cell interaction mechanism is not confined to the developing nervous system. In addition, recent studies have shown that elucidating the mechanism of Notch signaling and its role in the brain is important for our understanding of neurological disorders such as Alzheimer's disease and cerebral arteriopathy CADASIL.
More details
Series
Edition
2002 ed.
Language
English
Place of publication
Berlin
Germany
Publishing group
Springer Berlin
Target group
Professional and scholarly
Research
Illustrations
XVI, 158 p.
Dimensions
Height: 241 mm
Width: 160 mm
Thickness: 16 mm
Weight
475 gr
ISBN-13
978-3-540-43073-5 (9783540430735)
DOI
10.1007/978-3-642-55996-9
Schweitzer Classification
Other editions
Additional editions
A. Israel | B. de Strooper | F. Checler
Notch from Neurodevelopment to Neurodegeneration: Keeping the Fate
Book
10/2012
Springer
€160.49
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Content
Regulated Intramembrane Proteolysis - New Lessons from Lipid Metabolism and the Unfolded Protein Response.- Notch Signaling in the Brain: More than Just a Developmental Story.- Control of Notch Activity by the Ubiquitin-Proteasome Pathway.- A Presenilin-Dependent S3-Like ?-Secretase Cleavage of the ?-Amyloid Precursor Protein.- New Non-Peptidic Inhibitors of ?-Secretase Abolish A? Production Without Modifying Notch Cleavage.- Presenilins, APP, and Notch: Proteolysis from Womb to Tomb.- Missorting of the Dendritic Cell Adhesion Molecule Telencephalin in Presenilin-Deficient Neurons.- ?APP Processing, its Biology and Alzheimer's Disease.- Further Analysis of the Nicastrin: Presenilin Complex.- PS1 Interacts With and Facilitates ?-Catenin Turnover.- ?-Catenin, Presenilin, and the Synaptic-Adherens Junction Complex.- Vascular Smooth Muscle Cells Are the Primary Target of the Events Leading from Notch3 Mutations to CADASIL.