Degenerative terminals of the perforant pathway are human α-synuclein-immunoreactive in the hippocampus of patients with diffuse Lewy body disease

被引：62

作者：

Iseki, E

Marui, W

Kosaka, K

Akiyama, H

Ueda, K

Iwatsubo, T

机构：

[1] Yokohama City Univ, Sch Med, Dept Psychiat, Kanazawa Ku, Yokohama, Kanagawa 2360004, Japan

[2] Tokyo Inst Psychiat, Setagaya Ku, Tokyo 1560057, Japan

[3] Univ Tokyo, Grad Sch Pharmaceut Sci, Dept Neuropathol & Neurosci, Bunkyo Ku, Tokyo 1130033, Japan

来源：

NEUROSCIENCE LETTERS | 1998年 / 258卷 / 02期

关键词：

diffuse lewy body disease; hippocampus; perforant pathway; alpha-synuclein; ubiquitin; immunohistochemistry;

D O I：

10.1016/S0304-3940(98)00856-8

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

We investigated the hippocampal pathology in diffuse Lewy body disease (DLBD) using alpha-synuclein immunohistochemistry. Ubiquitin-positive intrahippocampal structures caused by the degeneration of terminal axons of the perforant pathway were observed to be alpha-synuclein immunoreactive. These alpha-synuclein-positive degenerative terminals contained granulo-filamentous or vesiculo-tubular components similar to those of Lewy bodies (LB) immunoelectron microscopically, suggesting that alpha-synuclein may abnormally aggregate into filamentous or membranous cytoskeletal components including neurofilaments and synaptic vesicles in DLBD. A 'dying back' degenerating process due to a blockage of axonal transport may explain why the degenerative terminals and LB share similar alpha-synuclein-positive components, but the origin cells of the perforant pathway contain only a few LB. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：81 / 84

页数：4

共 18 条

[1] Baba M, 1998, AM J PATHOL, V152, P879
[2] DICKSON DW, 1994, ACTA NEUROPATHOL, V87, P269
[3] PHASE AND ELECTRON MICROSCOPIC OBSERVATIONS OF LEWY BODIES AND MELANIN GRANULES IN SUBSTANTIA NIGRA AND LOCUS CAERULEUS IN PARKINSONS DISEASE
DUFFY, PE
TENNYSON, VM
[J]. JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1965, 24 (03) : 398 - +
[4] PERFORANT PATHWAY CHANGES AND THE MEMORY IMPAIRMENT OF ALZHEIMERS-DISEASE
HYMAN, BT
VANHOESEN, GW
KROMER, LJ
DAMASIO, AR
[J]. ANNALS OF NEUROLOGY, 1986, 20 (04) : 472 - 481
[5] Hippocampal pathology in diffuse Lewy body disease using ubiquitin immunohistochemistry
Iseki, E
Li, F
Odawara, T
Kosaka, K
[J]. JOURNAL OF THE NEUROLOGICAL SCIENCES, 1997, 149 (02) : 165 - 169
[6] 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
[7] 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
[8] DIFFUSE LEWY BODY DISEASE IN JAPAN
KOSAKA, K
[J]. JOURNAL OF NEUROLOGY, 1990, 237 (03) : 197 - 204
[9] LEWY BODIES ARE UBIQUITINATED - A LIGHT AND ELECTRON-MICROSCOPIC IMMUNOCYTOCHEMICAL STUDY
KUZUHARA, S
MORI, H
IZUMIYAMA, N
YOSHIMURA, M
IHARA, Y
[J]. ACTA NEUROPATHOLOGICA, 1988, 75 (04) : 345 - 353
[10] Masliah E, 1996, AM J PATHOL, V148, P201

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