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

154 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)

Access to Document

10.1016/S0304-3940(01)02583-6

Fingerprint Dive into the research topics of 'Lithium inhibits amyloid secretion in COS7 cells transfected with amyloid precursor protein C100'. Together they form a unique fingerprint.

Cite this

@article{ec68c99d7a0e4c648e28a167369cf287,

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.",

keywords = "Alzheimer's disease, Amyloid, Glycogen synthase kinase-3β, Lithium",

author = "X. Sun and S. Sato and O. Murayama and M. Murayama and Park, {J. M.} and H. Yamaguchi and A. Takashima",

year = "2002",

month = mar,

day = "15",

doi = "10.1016/S0304-3940(01)02583-6",

language = "English (US)",

volume = "321",

pages = "61--64",

journal = "Neuroscience Letters",

issn = "0304-3940",

publisher = "Elsevier Ireland Ltd",

number = "1-2",

}

TY - JOUR

T1 - Lithium inhibits amyloid secretion in COS7 cells transfected with amyloid precursor protein C100

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

Y1 - 2002/3/15

N2 - 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.

AB - 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.

KW - Alzheimer's disease

KW - Amyloid

KW - Glycogen synthase kinase-3β

KW - Lithium

UR - http://www.scopus.com/inward/record.url?scp=0037087220&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037087220&partnerID=8YFLogxK

U2 - 10.1016/S0304-3940(01)02583-6

DO - 10.1016/S0304-3940(01)02583-6

M3 - Article

C2 - 11872257

AN - SCOPUS:0037087220

VL - 321

SP - 61

EP - 64

JO - Neuroscience Letters

JF - Neuroscience Letters

SN - 0304-3940

IS - 1-2

ER -

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

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Cite this