Notch from Neurodevelopment to Neurodegeneration: Keeping the Fate

1. Front Matter

   Pages I-XVI

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2. Regulated Intramembrane Proteolysis — New Lessons from Lipid Metabolism and the Unfolded Protein Response

   • R. B. Rawson

   Pages 1-17

3. Notch Signaling in the Brain: More than Just a Developmental Story

   • N. Šestan, P. Rakic

   Pages 19-40

4. Control of Notch Activity by the Ubiquitin-Proteasome Pathway

   • N. Gupta-Rossi, O. Le Bail, Ch. Brou, F. Logeat, E. Six, A. Israël

   Pages 41-58

5. A Presenilin Dependent S3-Like γ-Secretase Cleavage of the β-Amyloid Precursor Protein

   • H. Steiner, M. Sastre, G. Multhaup, D. B. Teplow, Ch. Haass

   Pages 59-61

6. New Non-Peptidic Inhibitors of γ-Secretase Abolish Aβ Production Without Modifying Notch Cleavage

   • A. Petit, F. Bihel, C. Alves da Costa, O. Pourquié, Y.-H. Suh, J.-L. Kraus et al.

   Pages 63-70

7. Presenilins, APP, and Notch: Proteolysis from Womb to Tomb

   • M. S. Wolfe, W. P. Esler, W. T. Kimberly, D. J. Selkoe

   Pages 71-87

8. Missorting of the Dendritic Cell Adhesion Molecule Telencephalin in Presenilin-Deficient Neurons

   • C. Esselens, V. Baert, C. Boeve, G. Snellings, P. Cupers, K. Craessaerts et al.

   Pages 89-99

9. βAPP Processing, its Biology and Alzheimer’s Disease

   • L. D’Adamio

   Pages 101-108

10. Further Analysis of the Nicastrin: Presenilin Complex

    • F. Chen, G. Yu, S. Arawaka, M. Nishimura, T. Kawarai, H. Yu et al.

    Pages 109-117

11. PS1 Interacts With and Facilitates β-Catenin Turnover

    • E. H. Koo, S. Soriano, D. E. Kang

    Pages 119-129

12. δ-Catenin, Presenilin, and the Synaptic-Adherens Junction Complex

    • K. S. Kosik, M. Medina, T. Ochiishi, M. C. Martinez, Q. Lu

    Pages 131-141

13. Vascular Smooth Muscle Cells Are the Primary Target of the Events Leading from Notch3 Mutations to CADASIL

    • A. Joutel, F. Andreux, A. Francois, V. Domenga, F. Chapon, C. Godfraind et al.

    Pages 143-156

14. Back Matter

    Pages 157-158

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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.

• ALzheimer's Disease
• Nervous System
• Proteolysis
• neurons
• nicastrin
• presenilin
• ubiquitin-proteasome pathway

• Fondation IPSEN, Pour la Recherche Thérapeutique, Paris Cedex 16, France

  Yves Christen

• Institut Pasteur, Unité de Biologie Moléculaire de l’Expression Génique URA 1773 CNRS, Paris Cedex 15, France

  Alain Israël

• Laboratory for Neuronal Cell Biology Center for Human Genetics, KUL-Gasthuisberg and Flanders Interuniversity Institute for Biotechnology, Leuven, Belgium

  Bart Strooper

• Institut de Pharmacologie, Moléculaire et Cellulaire CNRS UPR 411, Sophia Antipolis, Valbonne, France

  Frédéric Checler

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