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:220
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
    DALE, GE
    PROBST, A
    LUTHERT, P
    MARTIN, J
    ANDERTON, BH
    LEIGH, PN
    [J]. ACTA NEUROPATHOLOGICA, 1992, 83 (05) : 525 - 529
  • [3] THE SIGNIFICANCE OF THE LEWY BODY IN THE DIAGNOSIS OF IDIOPATHIC PARKINSONS-DISEASE
    GIBB, WRG
    LEES, AJ
    [J]. NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY, 1989, 15 (01) : 27 - 44
  • [4] NEURONAL INCLUSIONS OF PARKINSONS-DISEASE
    GIBB, WRG
    SCOTT, T
    LEES, AJ
    [J]. MOVEMENT DISORDERS, 1991, 6 (01) : 2 - 11
  • [5] NEURONAL INPUTS TO HIPPOCAMPAL-FORMATION IN ALZHEIMERS-DISEASE AND IN PARKINSONISM-DEMENTIA COMPLEX ON GUAM
    GOTO, S
    HIRANO, A
    [J]. 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
    HAYASHIDA, K
    OYANAGI, S
    MIZUTANI, Y
    YOKOCHI, M
    [J]. ACTA NEUROPATHOLOGICA, 1993, 85 (04) : 445 - 448
  • [7] REGIONAL SYNAPTIC PATHOLOGY IN ALZHEIMERS-DISEASE
    HONER, WG
    DICKSON, DW
    GLEESON, J
    DAVIES, P
    [J]. NEUROBIOLOGY OF AGING, 1992, 13 (03) : 375 - 382
  • [8] Changes in presynaptic protein NACP/α-synuclein in an ischemic gerbil hippocampus
    Ishimaru, H
    Uéda, K
    Takahashi, A
    Maruyama, Y
    [J]. 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
    IWAI, A
    MASLIAH, E
    YOSHIMOTO, M
    GE, NF
    FLANAGAN, L
    DESILVA, HAR
    KITTEL, A
    SAITOH, T
    [J]. NEURON, 1995, 14 (02) : 467 - 475
  • [10] IDENTIFICATION OF 2 DISTINCT SYNUCLEINS FROM HUMAN BRAIN
    JAKES, R
    SPILLANTINI, MG
    GOEDERT, M
    [J]. FEBS LETTERS, 1994, 345 (01) : 27 - 32