Abstract
Alzheimer disease (AD) is characterized by excessive deposition of amyloid β-peptides (Aβ peptides) in the form of senile plaques as well as neurofibrillary tangles (NFTs) in the brain. In the amyloidogenic pathway, the amyloid-β precursor protein (APP) is cleaved by β-secretase first, followed by γ-secretase cleavage producing therefore Aβ. This review summarizes the recent findings in the AD field and focuses on the different γ-secretase inhibitors that have been developed as a therapeutic approach toward AD.
Keywords: Alzheimer disease, amyloid βprecursor protein, amyloid β, γ-secretase, presenilins, γ-secretase inhibitors, nonsteroidal anti-inflammatory drugs
Current Pharmaceutical Design
Title: Gamma-Secretase as a Pharmacological Target in Alzheimer Disease Research: When, Why and How?
Volume: 12 Issue: 33
Author(s): Chewki Ziani-Cherif, Bachir Mostefa-Kara and Fatima Z. Brixi-Gormat
Affiliation:
Keywords: Alzheimer disease, amyloid βprecursor protein, amyloid β, γ-secretase, presenilins, γ-secretase inhibitors, nonsteroidal anti-inflammatory drugs
Abstract: Alzheimer disease (AD) is characterized by excessive deposition of amyloid β-peptides (Aβ peptides) in the form of senile plaques as well as neurofibrillary tangles (NFTs) in the brain. In the amyloidogenic pathway, the amyloid-β precursor protein (APP) is cleaved by β-secretase first, followed by γ-secretase cleavage producing therefore Aβ. This review summarizes the recent findings in the AD field and focuses on the different γ-secretase inhibitors that have been developed as a therapeutic approach toward AD.
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Ziani-Cherif Chewki, Mostefa-Kara Bachir and Brixi-Gormat Z. Fatima, Gamma-Secretase as a Pharmacological Target in Alzheimer Disease Research: When, Why and How?, Current Pharmaceutical Design 2006; 12 (33) . https://dx.doi.org/10.2174/138161206778792994
DOI https://dx.doi.org/10.2174/138161206778792994 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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