Quantitation of amyloid-β peptides in biological milieu using a novel homogeneous time-resolved fluorescence (HTRF) assay

被引：51

作者：

Clarke, EE ^{[1
]}

Shearman, MS ^{[1
]}

机构：

[1] Merck Sharp & Dohme Ltd, Neurosci Res Ctr, Res Labs, Dept Mol Biol, Harlow CM20 2QR, Essex, England

来源：

JOURNAL OF NEUROSCIENCE METHODS | 2000年 / 102卷 / 01期

关键词：

Alzheimer's disease; amyloid precursor protein;

D O I：

10.1016/S0165-0270(00)00280-6

中图分类号：

Q5 [生物化学];

学科分类号：

071010 ; 081704 ;

摘要：

Many of the recent advances in the understanding of the pathological processes underlying Alzheimer's disease have come about as a result of the development of assays that can specifically quantitate in biological milieu amyloid-beta (A beta) peptides ending at amino-acid positions Ala-42 (A beta(42)) and Val-40 (A beta(40)). The existing technologies, however, although proven in their utility are limited in their application with regards to sample manipulation and suitability for high-throughput screening. To overcome these limitations, in this report we describe the development of a novel homogeneous time-resolved fluorescence (HTRF) immunoassay for A beta(42) and A beta(40) peptides. This assay has the sensitivity selectivity and dynamic range to allow specific, direct quantitation of A beta peptides in cell culture medium, plasma, cerebrospinal fluid and brain tissue extracts, and has the major advantage of minimising sample manipulation and its inherent inaccuracies. (C) 2000 Elsevier Science B.V. All rights reserved.

引用

页码：61 / 68

页数：8

共 32 条

[21] The E280A presenilin 1 Alzheimer mutation produces increased A beta 42 deposition and severe cerebellar pathology [J].

Lemere, CA ;

Lopera, F ;

Kosik, KS ;

Lendon, CL ;

Ossa, J ;

Saido, TC ;

Yamaguchi, H ;

Ruiz, A ;

Martinez, A ;

Madrigal, L ;

Hincapie, L ;

Arango, JCL ;

Anthony, DC ;

Koo, EH ;

Goate, AM ;

Selkoe, DJ ;

Arango, JCV .

NATURE MEDICINE, 1996, 2 (10) :1146-1150

[22] CANDIDATE GENE FOR THE CHROMOSOME-1 FAMILIAL ALZHEIMERS-DISEASE LOCUS [J].

LEVYLAHAD, E ;

WASCO, W ;

POORKAJ, P ;

ROMANO, DM ;

OSHIMA, J ;

PETTINGELL, WH ;

YU, CE ;

JONDRO, PD ;

SCHMIDT, SD ;

WANG, K ;

CROWLEY, AC ;

FU, YH ;

GUENETTE, SY ;

GALAS, D ;

NEMENS, E ;

WIJSMAN, EM ;

BIRD, TD ;

SCHELLENBERG, GD ;

TANZI, RE .

SCIENCE, 1995, 269 (5226) :973-977

[23] REDUCTION OF BETA-AMYLOID PEPTIDE(42), IN THE CEREBROSPINAL-FLUID OF PATIENTS WITH ALZHEIMERS-DISEASE [J].

MOTTER, R ;

VIGOPELFREY, C ;

KHOLODENKO, D ;

BARBOUR, R ;

JOHNSONWOOD, K ;

GALASKO, D ;

CHANG, L ;

MILLER, B ;

CLARK, C ;

GREEN, R ;

OLSON, D ;

SOUTHWICK, P ;

WOLFERT, R ;

MUNROE, B ;

LIEBERBURG, I ;

SEUBERT, P ;

SCHENK, D .

ANNALS OF NEUROLOGY, 1995, 38 (04) :643-648

[24]

Sabbagh M.N., 1997, ALZHEIMERS DIS REV, V3, P1

[25] Secreted amyloid beta-protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease [J].

Scheuner, D ;

Eckman, C ;

Jensen, M ;

Song, X ;

Citron, M ;

Suzuki, N ;

Bird, TD ;

Hardy, J ;

Hutton, M ;

Kukull, W ;

Larson, E ;

LevyLahad, E ;

Viitanen, M ;

Peskind, E ;

Poorkaj, P ;

Schellenberg, G ;

Tanzi, R ;

Wasco, W ;

Lannfelt, L ;

Selkoe, D ;

Younkin, S .

NATURE MEDICINE, 1996, 2 (08) :864-870

[26] Amyloid beta-protein and the genetics of Alzheimer's disease [J].

Selkoe, DJ .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (31) :18295-18298

[27] CLONING OF A GENE BEARING MISSENSE MUTATIONS IN EARLY-ONSET FAMILIAL ALZHEIMERS-DISEASE [J].

SHERRINGTON, R ;

ROGAEV, EI ;

LIANG, Y ;

ROGAEVA, EA ;

LEVESQUE, G ;

IKEDA, M ;

CHI, H ;

LIN, C ;

LI, G ;

HOLMAN, K ;

TSUDA, T ;

MAR, L ;

FONCIN, JF ;

BRUNI, AC ;

MONTESI, MP ;

SORBI, S ;

RAINERO, I ;

PINESSI, L ;

NEE, L ;

CHUMAKOV, I ;

POLLEN, D ;

BROOKES, A ;

SANSEAU, P ;

POLINSKY, RJ ;

WASCO, W ;

DASILVA, HAR ;

HAINES, JL ;

PERICAKVANCE, MA ;

TANZI, RE ;

ROSES, AD ;

FRASER, PE ;

ROMMENS, JM ;

STGEORGEHYSLOP, PH .

NATURE, 1995, 375 (6534) :754-760

[28] AN INCREASED PERCENTAGE OF LONG AMYLOID-BETA PROTEIN SECRETED BY FAMILIAL AMYLOID-BETA PROTEIN-PRECURSOR (BETA-APP(717)) MUTANTS [J].

SUZUKI, N ;

CHEUNG, TT ;

CAI, XD ;

ODAKA, A ;

OTVOS, L ;

ECKMAN, C ;

GOLDE, TE ;

YOUNKIN, SG .

SCIENCE, 1994, 264 (5163) :1336-1340

[29] Metabolism of the ''Swedish'' amyloid precursor protein variant in neuro2a (N2a) cells - Evidence that cleavage at the ''beta-secretase'' site occurs in the Golgi apparatus [J].

Thinakaran, G ;

Teplow, DB ;

Siman, R ;

Greenberg, B ;

Sisodia, SS .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (16) :9390-9397

[30] Intracellular and secreted Alzheimer beta-amyloid species are generated by distinct mechanisms in cultured hippocampal neurons [J].

Tienari, PJ ;

Ida, N ;

Ikonen, E ;

Simons, M ;

Weidemann, A ;

Multhaup, G ;

Masters, CL ;

Dotti, CG ;

Beyreuther, K .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (08) :4125-4130

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