ULTRASTRUCTURAL-LOCALIZATION OF COMPLEMENT MEMBRANE ATTACK COMPLEX (MAC)-LIKE IMMUNOREACTIVITY IN BRAINS OF PATIENTS WITH ALZHEIMERS-DISEASE

被引：88

作者：

ITAGAKI, S

AKIYAMA, H

SAITO, H

MCGEER, PL

机构：

[1] UNIV BRITISH COLUMBIA, KINSMEN LAB NEUROL RES, VANCOUVER V6T 1W5, BC, CANADA

[2] HIBARIGAOKA HOSP, DEPT PSYCHIAT, HARAMATI, FUKUSHIMA 975, JAPAN

[3] TOKYO INST PSYCHIAT, TOKYO 156, JAPAN

[4] FUKUSHIMA MED COLL, DEPT NEUROPSYCHIAT, FUKUSHIMA 96012, JAPAN

来源：

BRAIN RESEARCH | 1994年 / 645卷 / 1-2期

关键词：

COMPLEMENT; ALZHEIMERS DISEASE; MEMBRANE ATTACK COMPLEX; ULTRASTRUCTURE; TANGLE;

D O I：

10.1016/0006-8993(94)91640-3

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The membrane attack complex (MAC) of complement, also known as C5b-9, was localized in Alzheimer's disease (AD) brain by immunoelectron microscopy using a monoclonal antibody to a neoantigenic epitope of soluble C5b-9 (SC5b-9). Immunopositivity was detected in association with lamellated bodies in the neuronal cytoplasm, lipofuscin granules, lysosomes and neurofibrillary tangles (NFTs). Such intracellular localization of MAC-like immunoreactive (MAC-LI) staining suggests that neurons remove membrane-inserted MAC fragments by endocytosis. These endocytosed membrane fragments then proceed by retrograde transport to the perikaryon for lysosomal degradation. Attachment to the abnormal cytoskeletal proteins found in neurofibrillary tangles also occurs. The results provide further evidence that complement-mediated injury of neurons plays a part in the pathophysiology of AD.

引用

页码：78 / 84

页数：7

共 34 条

[21] REACTIVE MICROGLIA IN PATIENTS WITH SENILE DEMENTIA OF ALZHEIMER TYPE ARE POSITIVE FOR THE HISTOCOMPATIBILITY GLYCOPROTEIN HLA-DR [J].