Immunoelectron-microscopic demonstration of NACP/α-synuclein-epitopes on the filamentous component of Lewy bodies in Parkinson's disease and in dementia with Lewy bodies

被引:221
作者
Arima, K
Uéda, K
Sunohara, N
Hirai, S
Izumiyama, Y
Tonozuka-Uehara, H
Kawai, M
机构
[1] Tokyo Inst Psychiat, Dept Ultrastruct & Histochem, Setagaya Ku, Tokyo 1568585, Japan
[2] NCNP, Natl Ctr Hosp Mental Nervous & Muscular Disorder, Dept Lab Med, Kodaira, Tokyo 1878551, Japan
[3] Tokyo Inst Psychiat, Dept Neurochem, Tokyo 1568585, Japan
[4] NCNP, Natl Ctr Hosp Mental Nervous & Muscular Disorders, Dept Neurol, Kodaira, Tokyo 1878551, Japan
[5] NCNP, Natl Ctr Hosp Mental Nervous & Muscular Disorders, Dept Psychiat, Kodaira, Tokyo 1878551, Japan
关键词
Lewy body; NACP; synuclein; Parkinson's disease; filament aggregation; neuronal degeneration;
D O I
10.1016/S0006-8993(98)00734-3
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We examined brains from Parkinson's disease and from dementia with Lewy bodies (LBs) by using antibodies to NACP/alpha-synuclein. Immunohistochemically, all of the antibodies against the amino-terminal region, NAC domain, and carboxyl-terminal region of NACP labeled not only LBs, pale bodies (PBs), and dystrophic neurites, but also fine thread-like structures in the neuronal perikarya (perikaryal threads) in the hypothalamus and brainstem nuclei. On electron microscopy, immunoreactive products were found to label the 9 to 12 nm-thick filamentous component (LB-filaments) of LBs, PBs, and perikaryal threads. The NACP-immunoreactive perikaryal threads, consisting of small bundles of LB-filaments and randomly oriented LB-filaments, presumably represent an initial stage of LB- or PB-formation. The present study indicates that the entire molecule of NACP is involved in the neuronal filament-aggregating processes of LB disorders. (C) 1998 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:93 / 100
页数:8
相关论文
共 19 条
[1]  
Baba M, 1998, AM J PATHOL, V152, P879
[2]   RELATIONSHIPS BETWEEN LEWY BODIES AND PALE BODIES IN PARKINSONS-DISEASE [J].
DALE, GE ;
PROBST, A ;
LUTHERT, P ;
MARTIN, J ;
ANDERTON, BH ;
LEIGH, PN .
ACTA NEUROPATHOLOGICA, 1992, 83 (05) :525-529
[3]   THE SIGNIFICANCE OF THE LEWY BODY IN THE DIAGNOSIS OF IDIOPATHIC PARKINSONS-DISEASE [J].
GIBB, WRG ;
LEES, AJ .
NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY, 1989, 15 (01) :27-44
[4]   NEURONAL INCLUSIONS OF PARKINSONS-DISEASE [J].
GIBB, WRG ;
SCOTT, T ;
LEES, AJ .
MOVEMENT DISORDERS, 1991, 6 (01) :2-11
[5]   NEURONAL INPUTS TO HIPPOCAMPAL-FORMATION IN ALZHEIMERS-DISEASE AND IN PARKINSONISM-DEMENTIA COMPLEX ON GUAM [J].
GOTO, S ;
HIRANO, A .
ACTA NEUROPATHOLOGICA, 1990, 79 (05) :545-550
[6]   AN EARLY CYTOPLASMIC CHANGE BEFORE LEWY BODY MATURATION - AN ULTRASTRUCTURAL-STUDY OF THE SUBSTANTIA-NIGRA FROM AN AUTOPSY CASE OF JUVENILE PARKINSONISM [J].
HAYASHIDA, K ;
OYANAGI, S ;
MIZUTANI, Y ;
YOKOCHI, M .
ACTA NEUROPATHOLOGICA, 1993, 85 (04) :445-448
[7]   REGIONAL SYNAPTIC PATHOLOGY IN ALZHEIMERS-DISEASE [J].
HONER, WG ;
DICKSON, DW ;
GLEESON, J ;
DAVIES, P .
NEUROBIOLOGY OF AGING, 1992, 13 (03) :375-382
[8]   Changes in presynaptic protein NACP/α-synuclein in an ischemic gerbil hippocampus [J].
Ishimaru, H ;
Uéda, K ;
Takahashi, A ;
Maruyama, Y .
BRAIN RESEARCH, 1998, 788 (1-2) :311-314
[9]   THE PRECURSOR PROTEIN OF NON-A-BETA COMPONENT OF ALZHEIMERS-DISEASE AMYLOID IS A PRESYNAPTIC PROTEIN OF THE CENTRAL-NERVOUS-SYSTEM [J].
IWAI, A ;
MASLIAH, E ;
YOSHIMOTO, M ;
GE, NF ;
FLANAGAN, L ;
DESILVA, HAR ;
KITTEL, A ;
SAITOH, T .
NEURON, 1995, 14 (02) :467-475
[10]   IDENTIFICATION OF 2 DISTINCT SYNUCLEINS FROM HUMAN BRAIN [J].
JAKES, R ;
SPILLANTINI, MG ;
GOEDERT, M .
FEBS LETTERS, 1994, 345 (01) :27-32