α-Synuclein accumulates in Lewy bodies in Parkinson's disease and dementia with Lewy bodies but not in Alzheimer's disease β-amyloid plaque cores

被引：85

作者：

Bayer, TA

Jäkälä, P

Hartmann, T

Havas, L

McLean, C

Culvenor, JG

Li, QX

Masters, CL

Falkai, P

Beyreuther, K

机构：

[1] Univ Bonn, Med Ctr, Dept Psychiat, D-53105 Bonn, Germany

[2] ZMBH, D-69120 Heidelberg, Germany

[3] Univ Kuopio, Dept Neurosci & Neurol, FIN-70211 Kuopio, Finland

[4] Kuopio Univ Hosp, Dept Neurosci & Neurol, Kuopio 70211, Finland

[5] Inst Nervous & Mental Dis, Neuropathol Lab, H-1281 Budapest, Hungary

[6] Univ Melbourne, Dept Pathol, Parkville, Vic 3052, Australia

来源：

NEUROSCIENCE LETTERS | 1999年 / 266卷 / 03期

基金：

芬兰科学院;

关键词：

Alzheimer's disease; Parkinson; post-mortem human brain; senile plaques; lewy bodies;

D O I：

10.1016/S0304-3940(99)00311-0

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

A growing body of evidence suggests that the non-Ap component of Alzheimer's disease amyloid precursor protein (NACP) or alpha-synuclein contributes to the neurodegenerative processes in Alzheimer's disease (AD), Parkinson's disease (PD) and dementia with Lewy bodies (DLB). In the present study antisera to the N terminus and the NAC domain of the alpha-synuclein protein were employed to elucidate the expression pattern in brains of patients with AD, PD, DLB and control specimen. alpha-Synuclein exhibited an overall punctuate expression profile compatible with a synaptic function. Interestingly, while Lewy bodies were strongly immunoreactive, none of the alpha-synuclein antisera revealed staining in mature beta-amyloid plaques in AD. These observations suggest that alpha-synuclein does not contribute to late neurodegenerative processes in AD brains. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：213 / 216

页数：4

共 25 条

[1] 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 [J].