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
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
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页码:213 / 216
页数:4
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