Acta Neuropathologica

, Volume 99, Issue 1, pp 14–20

NACP/α-synuclein-positive filamentous inclusions in astrocytes and oligodendrocytes of Parkinson’s disease brains

Authors

  • K. Wakabayashi
    • Brain Disease Research Center, Brain Research Institute, Niigata University, 1 Asahimachi, Niigata 951-8585, Japan e-mail: koichi@bri.niigata-u.ac.jp Tel.: +81-25-227-0673, Fax: +81-25-227-0817
  • S. Hayashi
    • Department of Pathology, Brain Research Institute, Niigata University, 1 Asahimachi, Niigata 951-8585, Japan
  • M. Yoshimoto
    • Molecular Biology Laboratory, Medicinal Research Laboratories, Taisho Pharmaceutical Co. Ltd., Ohmiya, Saitama 330-0031, Japan
  • H. Kudo
    • Molecular Biology Laboratory, Medicinal Research Laboratories, Taisho Pharmaceutical Co. Ltd., Ohmiya, Saitama 330-0031, Japan
  • H. Takahashi
    • Department of Pathology, Brain Research Institute, Niigata University, 1 Asahimachi, Niigata 951-8585, Japan
Regular paper

DOI: 10.1007/PL00007400

Cite this article as:
Wakabayashi, K., Hayashi, S., Yoshimoto, M. et al. Acta Neuropathol (2000) 99: 14. doi:10.1007/PL00007400

Abstract

The precursor of the non-Aβ component of Alzheimer’s disease amyloid (NACP), also called α-synuclein, is a major component of Lewy bodies in Parkinson’s disease (PD) as well as of neuronal and oligodendroglial cytoplasmic inclusions in multiple system atrophy. We previously reported argyrophilic, tau-negative glial inclusions in the midbrains of patients with PD and have now conducted immunocytochemical and ultrastructural examinations. The PD glial inclusions also are immunoreactive for NACP/α-synuclein, but not for β-synuclein, and ultrastructurally are composed of filamentous structures about 25–40 nm in diameter. Double immunolabeling showed that the inclusions were present in both astrocytic and oligodendroglial cells. They were located within the substantia nigra in 13 of 30 patients with PD and outside the nigra in 24. The number of inclusions was correlated with the severity of nigral neuronal loss. These findings indicate that abnormal accumulation of NACP/α-synuclein in glial cells is a pathological feature of PD related to its progression.

Key wordsα-SynucleinAstrocyteOligodendrocyteGlial inclusionParkinson’s disease

Copyright information

© Springer-Verlag Berlin Heidelberg 2000