Reciprocal accumulation of β-synuclein in α-synuclein lesions in multiple system atrophy

被引:20
作者
Mori, F
Nishie, M
Yoshimoto, M
Takahashi, H
Wakabayashi, K
机构
[1] Hirosaki Univ, Sch Med, Inst Brain Sci, Dept Neuropathol, Hirosaki, Aomori 0368562, Japan
[2] Taisho Pharmaceut Co Ltd, Med Res Labs, Mol Biol Lab, Saitama, Japan
[3] Niigata Univ, Brain Res Inst, Dept Pathol, Niigata, Japan
关键词
inclusion body; multiple system atrophy; protein aggregation; alpha-synuclein; beta-synuclein;
D O I
10.1097/00001756-200310060-00005
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
alpha-Synuclein is a major component of neuronal and glial cytoplasmic inclusions in multiple system atrophy (MSA), one of the alpha-synucleinopathies. Recent studies have shown that [ synuclein, a homolog of alpha-synuclein, inhibits alpha-synuclein aggregation in vitro. We immunohistochemically examined the MSA brain, using specific antibodies against alpha-synuclein and beta-synuclein. alpha-synuclein-positive filamentous aggregates were frequently found in neurons in the pontine and inferior olivary nuclei. No abnormal accumulation of alpha-synuclein was noted in Purkinje cells. In contrast, beta-synuclein accumulation occurred extensively in Purkinje cells, and only minimally in pontine and olivary neurons. Thus, neuronal a-synuclein inclusions appear to occur only rarely in neurons in which beta-synuclein accumulates. These findings support the possibility that beta-synuclein is a negative regulator of alpha-synuclein aggregation.
引用
收藏
页码:1783 / 1786
页数:4
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