Tau immunoreactivity in glial cytoplasmic inclusions in multiple system atrophy

被引:32
作者
Takeda, A
Arai, N
Komori, T
Iseki, E
Kato, S
Oda, M
机构
[1] TOKYO METROPOLITAN INST NEUROSCI,DEPT CLIN NEUROPATHOL,FUCHU,TOKYO 183,JAPAN
[2] YOKOHAMA CITY UNIV,SCH MED,DEPT PSYCHIAT,YOKOHAMA,KANAGAWA 232,JAPAN
[3] TOKYO METROPOLITAN NEUROL HOSP,DEPT NEUROL,TOKYO,JAPAN
[4] TOKYO METROPOLITAN NEUROL HOSP,DEPT PATHOL,TOKYO,JAPAN
关键词
glial cytoplasmic inclusions; multiple system atrophy; tau; microtubule-associated proteins; coiled bodies;
D O I
10.1016/S0304-3940(97)00676-9
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
In order to clarify the manner and significance of tau expression in glial cytoplasmic inclusions (GCls), ubiquitinated oligodendroglial abnormal structures in multiple system atrophy (MSA), an immunohistochemical study was carried out in the lesions of the pontine nuclei of 10 cases of MSA using antibodies against various epitope locations of tau protein. As a result, tau-2 was constantly but weakly positive in ubiquitinated GCls in each case (from 28.6 to 66.7%). However, tau-2-immunoreactivity in GCls was not correlated to the density of ubiquitin-positive GCls or preserved pontine neurons. Antibodies against tau proteins of N-terminal or C-terminal failed to label GCls, although a few number of GCls were occasionally positive for tau-l after dephosphorylation. In comparison with the knowledge on tau-immunoreactivity of coiled bodies (CBs) in oligodendroglia in progressive supranuclear palsy (PSP) or corticobasal degeneration, GCls are quite different from CBs which have a wide range of epitope location of tau proteins, including N-terminal and C-terminal. This study suggests that expression of tau proteins in GCls is not related to the essential neurodegenerative process in MSA but induced by non-specific stress in oligodendroglia, unlike CB in various 'tau diseases' such as PSP. (C) 1997 Elsevier Science Ireland Ltd.
引用
收藏
页码:63 / 66
页数:4
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