Activation of microglia in the brains of humans with heart disease and hypercholesterolemic rabbits

被引:141
作者
Streit, WJ [1 ]
Sparks, DL [1 ]
机构
[1] UNIV KENTUCKY,SANDERS BROWN CTR AGING,KENTUCKY STATE MED EXAMINERS PROGRAM,JUSTICE CABINET,LEXINGTON,KY 40536
来源
JOURNAL OF MOLECULAR MEDICINE-JMM | 1997年 / 75卷 / 02期
关键词
Alzheimer's disease; aging; senile plaques; amyloid; high serum cholesterol; lectin staining;
D O I
10.1007/s001090050097
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Activated microglial cells are concentrated in senile plaques characteristic of Alzheimer's disease, Such accumulations of activated microglia may contribute towards neurodegeneratiun via production of cytokines and free radicals. Studies suggesting a link between Alzheimer's disease and heart disease led us to study microglia immunohistochemically, using monoclonal antibody LN-3, in age-matched nondemented humans with and without heart disease. Using a qualitative staging system for assessing morphological changes occurring in microglia, we found higher microglial activation in the blains of subjects with heart disease than in those without it. Lectin histochemical examination of brains from rabbits maintained on a high-cholesterol diet also revealed increased microglial activation and leukocyte infiltration. Collectively our observations from humans and rabbits suggest that hypercholesterolemia and heart disease accelerate brain aging, and that the formation of senile plaques may be the end result of progressive microglial activation that occurs with aging.
引用
收藏
页码:130 / 138
页数:9
相关论文
共 30 条
[1]   CYTOTOXICITY OF MICROGLIA [J].
BANATI, RB ;
GEHRMANN, J ;
SCHUBERT, P ;
KREUTZBERG, GW .
GLIA, 1993, 7 (01) :111-118
[2]   CARDIOVASCULAR-DISEASE AND DISTRIBUTION OF COGNITIVE FUNCTION IN ELDERLY PEOPLE - THE ROTTERDAM STUDY [J].
BRETELER, MMB ;
CLAUS, JJ ;
GROBBEE, DE ;
HOFMAN, A .
BRITISH MEDICAL JOURNAL, 1994, 308 (6944) :1604-1608
[3]  
BURGER PC, 1973, AM J PATHOL, V73, P457
[4]   PRODUCTION OF SUPEROXIDE ANIONS BY A CNS MACROPHAGE, THE MICROGLIA [J].
COLTON, CA ;
GILBERT, DL .
FEBS LETTERS, 1987, 223 (02) :284-288
[5]   ABNORMAL PRODUCTION OF INTERLEUKIN-1 BY MICROGLIA FROM TRISOMY-16 MICE [J].
COLTON, CA ;
YAO, J ;
TAFFS, RE ;
KERI, JE ;
OSTERGRANITE, ML .
NEUROSCIENCE LETTERS, 1991, 132 (02) :270-274
[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]   MICROGLIA AND CYTOKINES IN NEUROLOGICAL DISEASE, WITH SPECIAL REFERENCE TO AIDS AND ALZHEIMERS-DISEASE [J].
DICKSON, DW ;
LEE, SC ;
MATTIACE, LA ;
YEN, SHC ;
BROSNAN, C .
GLIA, 1993, 7 (01) :75-83
[8]   Microglia: Immune Network in the CNS [J].
Graeber, Manuel B. ;
Streit, Wotfgang J. .
BRAIN PATHOLOGY, 1990, 1 (01) :2-5
[9]  
GRIFFIN WST, 1989, P NATL ACAD SCI USA, V86, P7611
[10]   SYNTHETIC ALZHEIMER AMYLOID BETA-A4 PEPTIDES ENHANCE PRODUCTION OF COMPLEMENT C3 COMPONENT BY CULTURED MICROGLIAL CELLS [J].
HAGA, S ;
IKEDA, K ;
SATO, M ;
ISHII, T .
BRAIN RESEARCH, 1993, 601 (1-2) :88-94