Lithium inhibits amyloid secretion in COS7 cells transfected with amyloid precursor protein C100

X. Sun; S. Sato; O. Murayama; M. Murayama; J. M. Park; H. Yamaguchi; A. Takashima

doi:10.1016/S0304-3940(01)02583-6

Lithium inhibits amyloid secretion in COS7 cells transfected with amyloid precursor protein C100

X. Sun, S. Sato, O. Murayama, M. Murayama, J. M. Park, H. Yamaguchi, A. Takashima

Research output: Contribution to journal › Article › peer-review

153 Scopus citations

Abstract

To examine the regulation of amyloid secretion in more detail, Aβ sandwich ELISAs with high sensitivity and specificity were developed. Using this technique, we measured Aβ secreted from COS7 cells transiently transfected with APP C100 in the presence of LiCl, a potent glycogen synthase kinase (GSK)-3β inhibitor. We found that both Aβx-40 and Aβx-42 secretion were reduced by LiCl treatment in a dose-dependent manner. Diminished amyloid secretion was associated with GSK-3β activity. These results suggest that GSK-3β might function as a possible mediator for regulating both amyloid deposition and tau pathology in Alzheimer's disease (AD), and that lithium should be re-evaluated as a candidate reagent for preventing AD pathology.

Original language	English (US)
Pages (from-to)	61-64
Number of pages	4
Journal	Neuroscience Letters
Volume	321
Issue number	1-2
DOIs	https://doi.org/10.1016/S0304-3940(01)02583-6
State	Published - Mar 15 2002
Externally published	Yes

Keywords

Alzheimer's disease
Amyloid
Glycogen synthase kinase-3β
Lithium

ASJC Scopus subject areas

Neuroscience(all)

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title = "Lithium inhibits amyloid secretion in COS7 cells transfected with amyloid precursor protein C100",

abstract = "To examine the regulation of amyloid secretion in more detail, Aβ sandwich ELISAs with high sensitivity and specificity were developed. Using this technique, we measured Aβ secreted from COS7 cells transiently transfected with APP C100 in the presence of LiCl, a potent glycogen synthase kinase (GSK)-3β inhibitor. We found that both Aβx-40 and Aβx-42 secretion were reduced by LiCl treatment in a dose-dependent manner. Diminished amyloid secretion was associated with GSK-3β activity. These results suggest that GSK-3β might function as a possible mediator for regulating both amyloid deposition and tau pathology in Alzheimer's disease (AD), and that lithium should be re-evaluated as a candidate reagent for preventing AD pathology.",

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AU - Sun, X.

AU - Sato, S.

AU - Murayama, O.

AU - Murayama, M.

AU - Park, J. M.

AU - Yamaguchi, H.

AU - Takashima, A.

PY - 2002/3/15

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