Expression and distribution of carboxypeptidase B in the hippocampal subregions of normal and Alzheimer's disease brain

被引:4
|
作者
Papp, H
Török, I
Matsumoto, A
Enomoto, T
Matsuyama, S
Kása, P
机构
[1] Univ Szeged, Alzheimers Dis Res Ctr, H-6720 Szeged, Hungary
[2] Elisabeth City Hosp, Hodmezovasarhely, Hungary
[3] Kobe Univ, Grad Sch Med, Div Cell Biol, Kobe, Hyogo 657, Japan
[4] Kobe Univ, Fac Human Dev, Div Sci Nat Environm, Kobe, Hyogo 657, Japan
[5] Kobe Univ, Grad Sch Med, Div Mol Pharmacol, Kobe, Hyogo 657, Japan
来源
ACTA BIOLOGICA HUNGARICA | 2003年 / 54卷 / 01期
关键词
carboxypeptidase B; Alzheimer's disease; hippocampus; neurofibrillary degeneration; amyloid-beta;
D O I
10.1556/ABiol.54.2003.1.6
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Earlier neurochemical studies suggested that human brain carboxypeptidase B may play a significant role in the degradation of amyloid-beta1-42 in the brain. Using an immunohistochemical technique we report here on the neuronal expression and distribution of this enzyme in the segments (CA1a, CA1b and CA1c) of the CA1 subfield and in area CA4 of the hippocampus in normal and Alzheimer's disease brain samples. Its distribution was compared with the appearance of neurofibrillary tangles in the same brain sample. For immunohistochemical localization of carboxypeptidase B, a specific C14-module antibody was applied, together with the Gallyas silver impregnation technique for the demonstration of neurofibrillary tangles. The results revealed that, in the control samples, most of the immunoreactivity appeared in segment CA1a in the pyramidal cells, less in segment CA1b and least in segment CA1c. In the Alzheimer's disease samples, there was no particular immunostaining in the neurons, but, a large number of silver-impregnated degenerated neurons appeared. The results support the suggestion that carboxypeptidase B may play a significant role in elimination of the intracellular accumulation and toxicity of amyloid-beta in the human brain and thereby protect the neurons from degeneration.
引用
收藏
页码:55 / 62
页数:8
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