BETA-AMYLOID PROTEIN INCREASES THE VULNERABILITY OF CULTURED CORTICAL-NEURONS TO EXCITOTOXIC DAMAGE

被引:621
作者
KOH, JY [1 ]
YANG, LL [1 ]
COTMAN, CW [1 ]
机构
[1] UNIV CALIF IRVINE,DEPT PSYCHOBIOL,IRVINE,CA 92717
关键词
Alzheimer's disease; Glutamate; Kainate; N-methyl-d-aspartate; Neurodegeneration; Neurotoxicity; Plaque;
D O I
10.1016/0006-8993(90)91355-K
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Glutamate neurotoxicity may be an underlying pathological mechanism contributing to neuronal cell loss in a variety of conditions including Alzheimer's disease (AD). In this study, we examined whether the β-amyloid protein found in the neuritic plaques of AD alters the susceptibility of neurons to excitotoxic damage. While mature cortical neurons exposed to β-amyloid protein for 2-4 days did not appear to be damaged, their vulnerability to low-intesity exposure to glutamate, N-methyl-d-aspartate, and kainate increased, suggesting that this mechanism may contribute to the neurodegeneration seen in AD. © 1990.
引用
收藏
页码:315 / 320
页数:6
相关论文
共 30 条
[11]   THE PRECURSOR OF ALZHEIMERS-DISEASE AMYLOID-A4 PROTEIN RESEMBLES A CELL-SURFACE RECEPTOR [J].
KANG, J ;
LEMAIRE, HG ;
UNTERBECK, A ;
SALBAUM, JM ;
MASTERS, CL ;
GRZESCHIK, KH ;
MULTHAUP, G ;
BEYREUTHER, K ;
MULLERHILL, B .
NATURE, 1987, 325 (6106) :733-736
[12]   ALZHEIMERS-DISEASE [J].
KATZMAN, R .
NEW ENGLAND JOURNAL OF MEDICINE, 1986, 314 (15) :964-973
[13]   NOVEL PRECURSOR OF ALZHEIMERS-DISEASE AMYLOID PROTEIN SHOWS PROTEASE INHIBITORY ACTIVITY [J].
KITAGUCHI, N ;
TAKAHASHI, Y ;
TOKUSHIMA, Y ;
SHIOJIRI, S ;
ITO, H .
NATURE, 1988, 331 (6156) :530-532
[14]   QUANTITATIVE-DETERMINATION OF GLUTAMATE MEDIATED CORTICAL NEURONAL INJURY IN CELL-CULTURE BY LACTATE-DEHYDROGENASE EFFLUX ASSAY [J].
KOH, JY ;
CHOI, DW .
JOURNAL OF NEUROSCIENCE METHODS, 1987, 20 (01) :83-90
[15]   VULNERABILITY OF CULTURED CORTICAL-NEURONS TO DAMAGE BY EXCITOTOXINS - DIFFERENTIAL SUSCEPTIBILITY OF NEURONS CONTAINING NADPH-DIAPHORASE [J].
KOH, JY ;
CHOI, DW .
JOURNAL OF NEUROSCIENCE, 1988, 8 (06) :2153-2163
[16]  
KURLAND LT, 1972, FED PROC, V31, P1540
[17]   CORRELATION BETWEEN SENILE PLAQUE AND NEUROFIBRILLARY TANGLE COUNTS IN CEREBRAL-CORTEX AND NEURONAL COUNTS IN CORTEX AND SUBCORTICAL STRUCTURES IN ALZHEIMERS-DISEASE [J].
MANN, DMA ;
YATES, PO ;
MARCYNIUK, B .
NEUROSCIENCE LETTERS, 1985, 56 (01) :51-55
[18]   GLUTAMATE DYSFUNCTION IN ALZHEIMERS-DISEASE - AN HYPOTHESIS [J].
MARAGOS, WF ;
GREENAMYRE, JT ;
PENNEY, JB ;
YOUNG, AB .
TRENDS IN NEUROSCIENCES, 1987, 10 (02) :65-68
[19]   NEURONAL ORIGIN OF A CEREBRAL AMYLOID - NEUROFIBRILLARY TANGLES OF ALZHEIMERS-DISEASE CONTAIN THE SAME PROTEIN AS THE AMYLOID OF PLAQUE CORES AND BLOOD-VESSELS [J].
MASTERS, CL ;
MULTHAUP, G ;
SIMMS, G ;
POTTGIESSER, J ;
MARTINS, RN ;
BEYREUTHER, K .
EMBO JOURNAL, 1985, 4 (11) :2757-2763
[20]  
MATTSON J, 1989, Society for Neuroscience Abstracts, V15, P1039