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Titolo:
Metabolic regulation of brain A beta by neprilysin
Autore:
Iwata, N; Tsubuki, S; Takaki, Y; Shirotani, K; Lu, B; Gerard, NP; Gerard, C; Hama, E; Lee, HJ; Saido, TC;
Indirizzi:
RIKEN, Brain Sci Inst, Lab Proteolyt Neurosci, Wako, Saitama 3510198, Japan RIKEN Wako Saitama Japan 3510198 t Neurosci, Wako, Saitama 3510198, Japan Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 h Med, Dept Pediat, Boston, MA 02115 USA Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA Harvard Univ BostonMA USA 02115 Sch Med, Dept Med, Boston, MA 02115 USA
Titolo Testata:
SCIENCE
fascicolo: 5521, volume: 292, anno: 2001,
pagine: 1550 - 1552
SICI:
0036-8075(20010525)292:5521<1550:MROBAB>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
FAMILIAL ALZHEIMERS-DISEASE; INSULIN-DEGRADING ENZYME; GENE; MICE; PROTEIN; IDENTIFICATION; PRESENILIN-1; REGION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Agriculture,Biology & Environmental Sciences
Life Sciences
Physical, Chemical & Earth Sciences
Citazioni:
29
Recensione:
Indirizzi per estratti:
Indirizzo: Saido, TC RIKEN, Brain Sci Inst, Lab Proteolyt Neurosci, Wako, Saitama 3510198, Japan RIKEN Wako Saitama Japan 3510198 , Wako, Saitama 3510198, Japan
Citazione:
N. Iwata et al., "Metabolic regulation of brain A beta by neprilysin", SCIENCE, 292(5521), 2001, pp. 1550-1552

Abstract

Amyloid beta peptide (A beta) the pathogenic agent of Alzheimer's disease (AD), is a physiological metabolite in the brain. We examined the role of neprilysin, a candidate A beta -degrading peptidase, in the metabolism usingneprilysin gene-disrupted mice. Neprilysin deficiency resulted in defects both in the degradation of exogenously administered A beta and in the metabolic suppression of the endogenous A beta Levels in a gene dose-dependent manner. The regional Levels of A beta in the neprilysin-deficient mouse brain were in the distinct order of hippocampus, cortex, thalamus/striatum, andcerebellum, where hippocampus has the highest Level and cerebellum the lowest, correlating with the vulnerability to A beta 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 ADdevelopment by promoting A beta accumulation.

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Documento generato il 02/04/20 alle ore 09:03:58