Abstract
The accumulation of the amyloid-beta peptide (Aβ) continues to emerge as a central factor in Alzheimers disease (AD). In recent years attention has been drawn to clearance mechanisms of Aβ as evidence suggests reduced clearance may be linked to late-onset AD. Direct degradation of Aβ by endopeptidases has emerged as one critical pathway of clearance. Of particular interest are endopeptidases that are sensitive to the neprilysin inhibitors thiorphan and phosphoramidon (i.e. “NEP-like”) as these inhibitors induce a dramatic increase in Aβ levels resulting in rapid plaque formation in wild-type rodents. This review focuses on neprilysin (NEP) and on another NEP-like endopeptidase termed neprilysin- 2 (NEP2). The involvement of these endopeptidases in AD and the state of their therapeutic development are discussed.
Keywords: Neprilysin, NEP2, Alzheimer's disease, endopeptidase
Current Alzheimer Research
Title: Diabetes NEP-Like Endopeptidases and Alzheimers Disease
Volume: 7 Issue: 3
Author(s): R.A. Marr and B.J. Spencer
Affiliation:
Keywords: Neprilysin, NEP2, Alzheimer's disease, endopeptidase
Abstract: The accumulation of the amyloid-beta peptide (Aβ) continues to emerge as a central factor in Alzheimers disease (AD). In recent years attention has been drawn to clearance mechanisms of Aβ as evidence suggests reduced clearance may be linked to late-onset AD. Direct degradation of Aβ by endopeptidases has emerged as one critical pathway of clearance. Of particular interest are endopeptidases that are sensitive to the neprilysin inhibitors thiorphan and phosphoramidon (i.e. “NEP-like”) as these inhibitors induce a dramatic increase in Aβ levels resulting in rapid plaque formation in wild-type rodents. This review focuses on neprilysin (NEP) and on another NEP-like endopeptidase termed neprilysin- 2 (NEP2). The involvement of these endopeptidases in AD and the state of their therapeutic development are discussed.
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Cite this article as:
Marr R.A. and Spencer B.J., Diabetes NEP-Like Endopeptidases and Alzheimers Disease, Current Alzheimer Research 2010; 7 (3) . https://dx.doi.org/10.2174/156720510791050849
DOI https://dx.doi.org/10.2174/156720510791050849 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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