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Leptin inhibits amyloid β-protein degradation through decrease of neprilysin expression in primary cultured astrocytes.

Abstract：

:Pathogenesis of Alzheimer's disease (AD) is characterized by accumulation of extracellular deposits of amyloid β-protein (Aβ) in the brain. The steady state level of Aβ in the brain is determined by the balance between its production and removal; the latter occurring through egress across blood and CSF barriers as well as Aβ degradation. The major Aβ-degrading enzymes in the brain are neprilysin (NEP) and insulin-degrading enzyme (IDE), which may promote Aβ deposition in patients with sporadic late-onset AD. Epidemiological studies have suggested an inverse relationship between the adipocytokine leptin levels and the onset of AD. However, the mechanisms underlying the relationship remain uncertain. We investigated whether leptin is associated with Aβ degradation by inducing NEP and IDE expression within primary cultured astrocytes. Leptin significantly decreased the expression of NEP but not IDE in a concentration- and time-dependent manner through the activation of extracellular signal-regulated kinase (ERK) in cultured rat astrocytes. Furthermore, leptin inhibited the degradation of exogenous Aβ in primary cultured astrocytes. These results suggest that leptin suppresses Aβ degradation by NEP through activation of ERK.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Yamamoto N,Tanida M,Ono Y,Kasahara R,Fujii Y,Ohora K,Suzuki K,Sobue K

doi

10.1016/j.bbrc.2014.01.168

subject

Has Abstract

pub_date

2014-02-28 00:00:00

pages

214-7

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(14)00211-3

journal_volume

445

pub_type

杂志文章

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