AMYLOID BETA-PEPTIDE IN CEREBROSPINAL-FLUID IN INDIVIDUALS WITH THE SWEDISH ALZHEIMER AMYLOID PRECURSOR PROTEIN MUTATION

被引：31

作者：

LANNFELT, L ^{[1
]}

BASUN, H ^{[1
]}

VIGOPELFREY, C ^{[1
]}

WAHLUND, LO ^{[1
]}

WINBLAD, B ^{[1
]}

LIEBERBURG, I ^{[1
]}

SCHENK, D ^{[1
]}

机构：

[1] ATHENA NEUROSCI INC,S SAN FRANCISCO,CA 94080

来源：

NEUROSCIENCE LETTERS | 1995年 / 199卷 / 03期

关键词：

ALZHEIMERS DISEASE; AMYLOID BETA-PEPTIDE; AMYLOID PRECURSOR PROTEIN; PATHOGENIC MUTATION; CEREBROSPINAL FLUID;

D O I：

10.1016/0304-3940(95)12059-D

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The neuropathological hallmarks of Alzheimer's disease (AD) are amyloid-containing plaques and neurofibrillary tangles. The main constituent of senile plaques is amyloid beta-peptide (A beta) and in recent years, pathogenic mutations in the amyloid precursor protein (APP) gene have been discovered in some AD families. The APP(670/671) mutation, found in a Swedish AD family, has revealed over-production of A beta as one pathogenic mechanism for the development of AD. In the present study we have used an immunoassay to measure A beta levels in cerebrospinal fluid (CSF) from APP(670/671) mutation-carriers and non-carriers. A correlation was seen between decrease in A beta levels and duration of disease although no difference was found in levels of A beta between the groups (14.5 +/- 3.3 ng/ml versus 14.9 +/- 2.3 ng/ml).

引用

收藏

页码：203 / 206

页数：4

相关论文

共 28 条

[11] FRAMING BETA-AMYLOID [J].

HARDY, J .

NATURE GENETICS, 1992, 1 (04) :233-234

[12] INCREASED CEREBROSPINAL-FLUID TAU IN PATIENTS WITH ALZHEIMERS-DISEASE [J].

JENSEN, M ;

BASUN, H ;

LANNFELT, L .

NEUROSCIENCE LETTERS, 1995, 186 (2-3) :189-191

[13] INCREASED BETA-AMYLOID RELEASE AND LEVELS OF AMYLOID PRECURSOR PROTEIN (APP) IN FIBROBLAST CELL-LINES FROM FAMILY MEMBERS WITH THE SWEDISH ALZHEIMERS-DISEASE APP670/671 MUTATION [J].

JOHNSTON, JA ;

COWBURN, RF ;

NORGREN, S ;

WIEHAGER, B ;

VENIZELOS, N ;

WINBLAD, B ;

VIGOPELFREY, C ;

SCHENK, D ;

LANNFELT, L ;

ONEILL, C .

FEBS LETTERS, 1994, 354 (03) :274-278

[14] LOW-FREQUENCY OF THE APP-670/671 MUTATION IN FAMILIAL ALZHEIMERS-DISEASE IN SWEDEN [J].

LANNFELT, L ;

VIITANEN, M ;

JOHANSSON, K ;

AXELMAN, K ;

LILIUS, L ;

ALMQVIST, E ;

WINBLAD, B .

NEUROSCIENCE LETTERS, 1993, 153 (01) :85-87

[15] AMYLOID PRECURSOR PROTEIN MUTATION CAUSES ALZHEIMERS-DISEASE IN A SWEDISH FAMILY [J].

LANNFELT, L ;

BOGDANOVIC, N ;

APPELGREN, H ;

AXELMAN, K ;

LILIUS, L ;

HANSSON, G ;

SCHENK, D ;

HARDY, J ;

WINBLAD, B .

NEUROSCIENCE LETTERS, 1994, 168 (1-2) :254-255

[16] APOPTOSIS IS INDUCED BY BETA-AMYLOID IN CULTURED CENTRAL-NERVOUS-SYSTEM NEURONS [J].

LOO, DT ;

COPANI, A ;

PIKE, CJ ;

WHITTEMORE, ER ;

WALENCEWICZ, AJ ;

COTMAN, CW .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (17) :7951-7955

[17]

MCKHANN G, 1984, NEUROLOGY, V34, P939, DOI 10.1212/WNL.34.7.939

[18] A PATHOGENIC MUTATION FOR PROBABLE ALZHEIMERS-DISEASE IN THE APP GENE AT THE N-TERMINUS OF BETA-AMYLOID [J].

MULLAN, M ;

CRAWFORD, F ;

AXELMAN, K ;

HOULDEN, H ;

LILIUS, L ;

WINBLAD, B ;

LANNFELT, L .

NATURE GENETICS, 1992, 1 (05) :345-347

[19] AMYLOID-BETA PROTEIN-LEVELS IN CEREBROSPINAL-FLUID ARE ELEVATED IN EARLY-ONSET ALZHEIMERS-DISEASE [J].

NAKAMURA, T ;

SHOJI, M ;

HARIGAYA, Y ;

WATANABE, M ;

HOSODA, K ;

CHEUNG, TT ;

SHAFFER, LM ;

GOLDE, TE ;

YOUNKIN, LH ;

YOUNKIN, SG ;

HIRAI, S .

ANNALS OF NEUROLOGY, 1994, 36 (06) :903-911

[20] CEREBROSPINAL-FLUID LEVELS OF AMYLOID BETA-PROTEIN IN ALZHEIMERS-DISEASE - INVERSE CORRELATION WITH SEVERITY OF DEMENTIA AND EFFECT OF APOLIPOPROTEIN-E GENOTYPE [J].

NITSCH, RM ;

REBECK, GW ;

DENG, MH ;

RICHARDSON, UI ;

TENNIS, M ;

SCHENK, DB ;

VIGOPELFREY, C ;

LIEBERBURG, I ;

WURTMAN, RJ ;

HYMAN, BT ;

GROWDON, JH .

ANNALS OF NEUROLOGY, 1995, 37 (04) :512-518