Etiology of sporadic Alzheimer’s disease: Somatostatin, neprilysin, and amyloid β peptide

We recently demonstrated that amyloid β peptide (Aβ) is catabolized primarily by a neutral endopeptidase, neprilysin, in the brain and that a neuropeptide, somatostatin (SST), regulates brain Aβ level via modulation of neprilysin activity. Because SST expression in the brain declines upon aging in v...

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Bibliographic Details
Published in:Medical hypotheses 2005, Vol.65 (3), p.498-500
Main Authors: Hama, E., Saido, T.C.
Format: Article
Language:English
Subjects:
Aging - physiology
Alzheimer Disease - etiology
Alzheimer Disease - metabolism
Amyloid beta-Peptides - metabolism
Humans
Neprilysin - antagonists & inhibitors
Neprilysin - metabolism
Peptide Fragments - metabolism
Risk Factors
Somatostatin - biosynthesis
Somatostatin - physiology
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Summary:We recently demonstrated that amyloid β peptide (Aβ) is catabolized primarily by a neutral endopeptidase, neprilysin, in the brain and that a neuropeptide, somatostatin (SST), regulates brain Aβ level via modulation of neprilysin activity. Because SST expression in the brain declines upon aging in various mammals including rodents, apes and humans, we hypothesize that the aging-dependent reduction of SST triggers accumulation of Aβ in the brain by suppressing neprilysin action. This hypothesis accounts for the fact that aging is the predominant risk factor for Sporadic Alzheimer’s disease.
ISSN:0306-9877
1532-2777
DOI:10.1016/j.mehy.2005.02.045