ABNORMAL ACCUMULATION OF PHOSPHOLIPASE C-DELTA IN FILAMENTOUS INCLUSIONS OF HUMAN NEURODEGENERATIVE DISEASES

被引:24
|
作者
SHIMOHAMA, S
PERRY, G
RICHEY, P
TAKENAWA, T
WHITEHOUSE, PJ
MIYOSHI, K
SUENAGA, T
MATSUMOTO, S
NISHIMURA, M
KIMURA, J
机构
[1] UNIV TOKYO,INST MED,DEPT ONCOBIOL,MINATO KU,TOKYO 108,JAPAN
[2] HYOGO MED SCH,DEPT PSYCHIAT,NISHINOMIYA,HYOGO 663,JAPAN
[3] KITANO HOSP,DEPT NEUROL,KITA KU,OSAKA 530,JAPAN
[4] CASE WESTERN RESERVE UNIV HOSP,INST PATHOL,DIV NEUROPATHOL,CLEVELAND,OH 44106
[5] CASE WESTERN RESERVE UNIV HOSP,DEPT NEUROL,CLEVELAND,OH 44106
关键词
PHOSPHOLIPASE C-DELTA; ALZHEIMERS DISEASE; PICKS DISEASE; PROGRESSIVE SUPRANUCLEAR PALSY; DIFFUSE LEWY BODY DISEASE; PARKINSONS DISEASE; IMMUNOCYTOCHEMISTRY;
D O I
10.1016/0304-3940(93)90591-8
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We have previously demonstrated that an antibody to phosphoinositide-specific phospholipase C (PLC) isozyme, PLC-delta, intensely stained neurofibrillary tangles (NFT) in the brain tissue of Alzheimer's disease (AD). This study was performed to determine if abnormal PLC-delta accumulation might be present in the filamentous inclusions of other neurodegenerative diseases. We found that the anti-PLC-delta antibody stained neuronal inclusions of Pick's disease, progressive supranuclear palsy and diffuse Lewy body disease while the inclusions of idiopathic Parkinson's disease lacked PLC-delta accumulation. These results suggest a possible role for PLC-delta interaction in the formation of intraneuronal filamentous inclusions in human neurodegenerative diseases.
引用
收藏
页码:183 / 186
页数:4
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