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Evidence that γ-secretase mediates oxidative stress-induced β-secretase expression in Alzheimer's disease

Title
Evidence that γ-secretase mediates oxidative stress-induced β-secretase expression in Alzheimer's disease
Authors
Jo D.-G.Arumugam T.V.Woo H.-N.Park J.-S.Tang S.-C.Mughal M.Hyun D.-H.Park J.-H.Choi Y.-H.Gwon A.-R.Camandola S.Cheng A.Cai H.Song W.Markesbery W.R.Mattson M.P.
Ewha Authors
현동훈
SCOPUS Author ID
현동훈scopus
Issue Date
2010
Journal Title
Neurobiology of Aging
ISSN
0197-4580JCR Link
Citation
vol. 31, no. 6, pp. 917 - 925
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
β-Secretase (BACE1), an enzyme responsible for the production of amyloid β-peptide (Aβ), is increased by oxidative stress and is elevated in the brains of patients with sporadic Alzheimer's disease (AD). Here, we show that oxidative stress fails to induce BACE1 expression in presenilin-1 (γ-secretase)-deficient cells and in normal cells treated with γ-secretase inhibitors. Oxidative stress-induced β-secretase activity and sAPPβ levels were suppressed by γ-secretase inhibitors. Levels of γ- and β-secretase activities were greater in brain tissue samples from AD patients compared to non-demented control subjects, and the elevated BACE1 level in the brains of 3xTgAD mice was reduced by treatment with a γ-secretase inhibitor. Our findings suggest that γ-secretase mediates oxidative stress-induced expression of BACE1 resulting in excessive Aβ production in AD. © 2008.
DOI
10.1016/j.neurobiolaging.2008.07.003
Appears in Collections:
자연과학대학 > 생명과학전공 > Journal papers
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