CHRYSAMINE-G BINDING TO ALZHEIMER AND CONTROL BRAIN - AUTOPSY STUDY OF A NEW AMYLOID PROBE

被引：112
作者：
KLUNK, WE [1 ]
DEBNATH, ML [1 ]
PETTEGREW, JW [1 ]
机构：
[1] UNIV PITTSBURGH,SCH MED,WESTERN PSYCHIAT INST & CLIN,DEPT PSYCHIAT,NEUROPHYS LAB,PITTSBURGH,PA 15261
来源：
NEUROBIOLOGY OF AGING | 1995年 / 16卷 / 04期
关键词：
ALZHEIMERS DISEASE; BETA-AMYLOID; NEUROFIBRILLARY TANGLES; CEREBROVASCULAR AMYLOID; DIAGNOSIS; SYNTHESIS; BLOOD-BRAIN BARRIER; DIAZO DYES; CONGO RED; CHRYSAMINE G; HUMAN BRAIN;
D O I：
10.1016/0197-4580(95)00058-M
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：
Chrysamine-G (CG) is a carboxylic acid analogue of Congo red, a histologic dye which stains amyloid. CG binds to the beta-amyloid protein of Alzheimer's disease (AD) in vitro and partitions into the brain of normal mice. In this study, we demonstrate increased binding of [C-14]CG to homogenates of several regions of AD brain as compared to control. The total binding of CG to AD brain was approximately two- to three-fold that of control brain. The cerebellum could be used as an internal standard for each brain as CG binding to cerebellum did not differ between AD and control. The binding of [C-14]CG correlated with numbers of senile plaques and neurofibrillary tangles. In addition, CG could be used to stain cerebrovascular amyloid in tissue sections. These results suggest that CG may prove useful as an in vivo probe of amyloid deposition in AD.
引用
收藏
页码：541 / 548
页数：8
相关论文
共 42 条
[1]   ENHANCED DETECTION OF CONGO-RED-POSITIVE AMYLOID DEPOSITS IN MUSCLE-FIBERS OF INCLUSION-BODY MYOSITIS AND BRAIN OF ALZHEIMERS-DISEASE USING FLUORESCENCE TECHNIQUE [J].
ASKANAS, V ;
ENGEL, WK ;
ALVAREZ, RB .
NEUROLOGY, 1993, 43 (06) :1265-1267
[2]   NEUROPATHOLOGICAL STAGING OF ALZHEIMER LESIONS AND INTELLECTUAL STATUS IN ALZHEIMERS AND PARKINSONS-DISEASE PATIENTS [J].
BANCHER, C ;
BRAAK, H ;
FISCHER, P ;
JELLINGER, KA .
NEUROSCIENCE LETTERS, 1993, 162 (1-2) :179-182
[3]  
BEDAUX FC, 1963, WEEKBLAD, V98, P189
[4]   ASSOCIATION BETWEEN QUANTITATIVE MEASURES OF DEMENTIA AND OF SENILE CHANGE IN CEREBRAL GREY MATTER OF ELDERLY SUBJECTS [J].
BLESSED, G ;
TOMLINSON, BE ;
ROTH, M .
BRITISH JOURNAL OF PSYCHIATRY, 1968, 114 (512) :797-+
[5]   NEUROPATHOLOGICAL STAGING OF ALZHEIMER-RELATED CHANGES [J].
BRAAK, H ;
BRAAK, E .
ACTA NEUROPATHOLOGICA, 1991, 82 (04) :239-259
[6]   GENE DOSE OF APOLIPOPROTEIN-E TYPE-4 ALLELE AND THE RISK OF ALZHEIMERS-DISEASE IN LATE-ONSET FAMILIES [J].
CORDER, EH ;
SAUNDERS, AM ;
STRITTMATTER, WJ ;
SCHMECHEL, DE ;
GASKELL, PC ;
SMALL, GW ;
ROSES, AD ;
HAINES, JL ;
PERICAKVANCE, MA .
SCIENCE, 1993, 261 (5123) :921-923
[7]  
FALLETBIANCO C, 1990, REV NEUROL, V146, P687
[8]  
GLENNER GG, 1981, ANN PATHOL, V1, P120
[9]   TAU-PROTEIN AND THE NEUROFIBRILLARY PATHOLOGY OF ALZHEIMERS-DISEASE [J].
GOEDERT, M .
TRENDS IN NEUROSCIENCES, 1993, 16 (11) :460-465
[10]   CLONING AND SEQUENCING OF THE CDNA-ENCODING A CORE PROTEIN OF THE PAIRED HELICAL FILAMENT OF ALZHEIMER-DISEASE - IDENTIFICATION AS THE MICROTUBULE-ASSOCIATED PROTEIN TAU [J].
GOEDERT, M ;
WISCHIK, CM ;
CROWTHER, RA ;
WALKER, JE ;
KLUG, A .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1988, 85 (11) :4051-4055
12345