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Absence of alpha-synuclein pathology in postencephalitic parkinsonism.

Abstract
Postencephalitic parkinsonism (PEP), a chronic complication of encephalitis lethargica, is a tauopathy characterized by multisystem neuronal loss and gliosis with widespread neurofibrillary lesions composed of both 3- and 4-repeat (3R and 4R) tau isoforms. Previous immunohistochemical studies in a small number of PEP cases demonstrated absence of Lewy bodies as well as the lack of other alpha-synuclein pathology, classifying PEP as a "pure" tauopathy. Neuropathologic examination of 10 brains with clinico-pathologically verified PEP confirmed widespread neurodegeneration in subcortical and brainstem areas associated with multifocal neurofibrillary pathology comprising both 3R and 4R tau. Very rare beta-amyloid deposits were observed in two elderly patients, while Lewy bodies and neurites or any other alpha-synuclein deposits were completely absent. The causes and molecular background of total absence of alpha-synuclein pathology in PEP, in contrast to most other tauopathies, remain as unknown as the pathogenesis of PEP.
AuthorsKurt A Jellinger
JournalActa neuropathologica (Acta Neuropathol) Vol. 118 Issue 3 Pg. 371-9 (Sep 2009) ISSN: 1432-0533 [Electronic] Germany
PMID19404653 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Amyloid beta-Peptides
  • alpha-Synuclein
Topics
  • Adult
  • Amyloid beta-Peptides (metabolism)
  • Brain (metabolism, pathology)
  • Brain Stem (metabolism, pathology)
  • Female
  • Humans
  • Immunohistochemistry
  • Male
  • Middle Aged
  • Nerve Degeneration
  • Neurons (metabolism)
  • Parkinson Disease, Postencephalitic (metabolism, pathology)
  • Tauopathies (metabolism, pathology)
  • alpha-Synuclein (metabolism)

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