Journal
NEURODEGENERATIVE DISEASES
Volume 7, Issue 1-3, Pages 50-55Publisher
KARGER
DOI: 10.1159/000283483
Keywords
Amyloid beta-peptides; Alzheimer's disease; Presenilin; Tumor suppressor p53; gamma-Secretase complex
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Funding
- Fondation pour la Recherche Medicale
- Conseil General des Alpes Maritimes
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Amyloid beta-peptides is the generic term for a set of hydrophobic peptides that accumulate in Alzheimer's disease (AD)-affected brains. These amyloid-beta peptide fragments are mainly generated by an enzymatic machinery referred to as gamma-secretase complex that is built up by the association of four distinct proteins, namely presenilin 1 (PS1) or PS2, nicastrin, Aph-1 and Pen-2. AD is also characterized by exacerbated cell death that appears linked to the tumor suppressor p53. Interestingly, all members of the gamma-secretase complex control p53-dependent cell death. On the other hand, p53 appears to be able to regulate directly or indirectly the expression and transcription of PS1, PS2 and Pen-2. This review will focus on the functional cross-talk between the members of the gamma-secretase complex and p53 and will discuss the putative implication of this oncogene in AD pathology. Copyright (C) 2010 S. Karger AG, Basel
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