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Tau immunoreactivity in glial cytoplasmic inclusions in multiple system atrophy.

作者信息

Takeda A, Arai N, Komori T, Iseki E, Kato S, Oda M

机构信息

Department of Clinical Neuropathology, Tokyo Metropolitan Institute for Neuroscience, Fuchu, Japan.

出版信息

Neurosci Lett. 1997 Sep 26;234(1):63-6. doi: 10.1016/s0304-3940(97)00676-9.

Abstract

In order to clarify the manner and significance of tau expression in glial cytoplasmic inclusions (GCIs), 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 GCIs in each case (from 28.6 to 66.7%). However, tau-2-immunoreactivity in GCIs was not correlated to the density of ubiquitin-positive GCIs or preserved pontine neurons. Antibodies against tau proteins of N-terminal or C-terminal failed to label GCIs, although a few number of GCIs were occasionally positive for tau-1 after dephosphorylation. In comparison with the knowledge on tau-immunoreactivity of coiled bodies (CBs) in oligodendroglia in progressive supranuclear palsy (PSP) or corticobasal degeneration, GCIs 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 GCIs 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.

摘要

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