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Metabolic Regulation of Brain Aβ by Neprilysin

Iwata, Nobuhisa, Tsubuki, Satoshi, Takaki, Yoshie, Shirotani, Keiro, Lu, Bao, Gerard, Norma P., Gerard, Craig, Hama, Emi, Lee, Hahn-Jun, Saido, Takaomi C.·2001·Science

DOI 10.1126/science.1059946

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Abstract

Amyloid β peptide (Aβ), the pathogenic agent of Alzheimer's disease (AD), is a physiological metabolite in the brain. We examined the role of neprilysin, a candidate Aβ-degrading peptidase, in the metabolism using neprilysin gene-disrupted mice. Neprilysin deficiency resulted in defects both in the degradation of exogenously administered Aβ and in the metabolic suppression of the endogenous Aβ levels in a gene dose-dependent manner. The regional levels of Aβ in the neprilysin-deficient mouse brain were in the distinct order of hippocampus, cortex, thalamus/striatum, and cerebellum, where hippocampus has the highest level and cerebellum the lowest, correlating with the vulnerability to Aβ deposition in brains of humans with AD. Our observations suggest that even partial down-regulation of neprilysin activity, which could be caused by aging, can contribute to AD development by promoting Aβ accumulation.

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“1086 Aβ degradation in the extracellular space can be accomplished by several enzymes, and published studies have mainly focused on the proteases neprilysin, insulysin (insulin-degrading enzyme), MMP2, MMP9, and tPA/plasmin (Iwata et al., 2001; Melchor et al., 2003; Song and Hersh, 2005; Eckman et al., 2006; Yan et al…”
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Authors: Iwata, N., Tsubuki, S., Takaki, Y., Shirotani, K., Lu, B., Gerard, N. P., Gerard, C., Hama, E., Lee, H.-J., & Saido, T. C.
Venue: Science
Publisher: American Association for the Advancement of Science (AAAS)
Published: 2001-05-25
Volume: 292
Issue: 5521
Pages: 1550-1552
ISSN: 0036-8075 (ISSN-L)
1095-9203
DOI: 10.1126/science.1059946
OpenAlex: W2030011352
Cited by: 961
References: 3
FWCI: 25.42
Type: journal article
Language: en
Open access: closed

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Metabolic Regulation of Brain Aβ by Neprilysin

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