The pentraxins: possible role in Alzheimer's disease and other innate inflammatory diseases

被引:71
作者
McGeer, EG [1 ]
Yasojima, K [1 ]
Schwab, C [1 ]
McGeer, PL [1 ]
机构
[1] Univ British Columbia, Dept Psychiat, Kinsmen Lab Neurol Res, Vancouver, BC V6T 1Z3, Canada
关键词
neurofibrillary tangles; senile plaques; C-reactive proteins; amyloid P; complement; mRNA; in situ hybridization;
D O I
10.1016/S0197-4580(01)00288-3
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Two short pentraxins, C-reactive protein and amyloid P, are found in association with the senile plaques and neurofibrillary tangles of Alzheimer disease (AD). Formerly thought to be made primarily if not solely in liver, recent work has shown that they are made not only in the brain but in other tissues such as heart and arteries. Their synthesis is markedly upregulated in affected brain regions in AD. Since they are known to activate the complement cascade in an antibody-independent fashion and chronic activation can cause destruction of host tissue, these pentraxins may be important initiators of an autodestructive process. As such, they may be prime targets for therapeutic intervention. (C) 2001 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:843 / 848
页数:6
相关论文
共 60 条
[41]  
Pietila KO, 1996, EUR HEART J, V17, P1345
[42]   C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women [J].
Ridker, PM ;
Hennekens, CH ;
Buring, JE ;
Rifai, N .
NEW ENGLAND JOURNAL OF MEDICINE, 2000, 342 (12) :836-843
[43]   ACUTE PHASE PROTEINS ARE PRESENT IN AMORPHOUS PLAQUES IN THE CEREBRAL BUT NOT IN THE CEREBELLAR CORTEX OF PATIENTS WITH ALZHEIMERS-DISEASE [J].
ROZEMULLER, JM ;
STAM, FC ;
EIKELENBOOM, P .
NEUROSCIENCE LETTERS, 1990, 119 (01) :75-78
[44]  
Schwab C, 1997, ACTA NEUROPATHOL, V93, P87
[45]   Dystrophic neurites are associated with early stage extracellular neurofibrillary tangles in the parkinsonism-dementia complex of Guam [J].
Schwab, C ;
Steele, JC ;
McGeer, PL .
ACTA NEUROPATHOLOGICA, 1997, 94 (05) :486-492
[46]   Neuronal expression of mRNAs for complement proteins of the classical pathway in Alzheimer brain [J].
Shen, Y ;
Li, R ;
McGeer, EG ;
McGeer, PL .
BRAIN RESEARCH, 1997, 769 (02) :391-395
[47]   Serum amyloid P is not present in amyloid β deposits of a transgenic animal model [J].
Shi, J ;
Perry, G ;
Aliev, G ;
Smith, MA ;
Ashe, KH ;
Friedland, RP .
NEUROREPORT, 1999, 10 (15) :3229-3232
[48]   CORPORA-AMYLACEA COULD BE AN INDICATOR OF NEURODEGENERATION [J].
SINGHRAO, SK ;
NEAL, JW ;
NEWMAN, GR .
NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY, 1993, 19 (03) :269-276
[49]   Risk of Alzheimer's disease and duration of NSAID use [J].
Stewart, WF ;
Kawas, C ;
Corrada, M ;
Metter, EJ .
NEUROLOGY, 1997, 48 (03) :626-632
[50]   C-reactive - Protein structural biology, gene expression, and host defense function [J].
Szalai, AJ ;
Agrawal, A ;
Greenhough, TJ ;
Volanakis, JE .
IMMUNOLOGIC RESEARCH, 1997, 16 (02) :127-136