Notch from Neurodevelopment to Neurodegeneration: Keeping the Fate / Edition 1

by A. Israel, B. de Strooper, F. Checler, Y. Christen

Overview

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.

Product Details

ISBN-13:	9783540430735
Publisher:	Springer Berlin Heidelberg
Publication date:	08/05/2002
Series:	Research and Perspectives in Alzheimer's Disease
Edition description:	2002
Pages:	158
Product dimensions:	6.10(w) x 9.25(h) x 0.02(d)

Table of Contents

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.