4.3 Article

Degeneration in Different Parkinsonian Syndromes Relates to Astrocyte Type and Astrocyte Protein Expression

Journal

JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
Volume 68, Issue 10, Pages 1073-1083

Publisher

OXFORD UNIV PRESS INC
DOI: 10.1097/NEN.0b013e3181b66f1b

Keywords

alpha-Synuclein; Astrocytes; Corticobasal degeneration; Multiple system atrophy; Parkin; Parkinson disease; Progressive supranuclear palsy; Tau

Funding

  1. Australian Postgraduate and Parkinson's NSW Scholar
  2. GlaxoSmithKline Australia Postgraduate
  3. National Health and Medical Research Council of Australia
  4. Sara Matheson Trust for Multiple System Atrophy (Margaret Watson Memorial Grant)
  5. Alzheimer's Research Trust
  6. BrainNet Europe II [LSHM-CT-2004-503039]
  7. National Health and Medical Research Council of Australia [282933]
  8. Queen Square Brain Bank
  9. Reta Lila Weston Institute for Neurological Studies and the Progressive Supranuclear Palsy (Europe) Association

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The reactive changes in different types of astrocytes were analyzed in parkinsonian syndromes in order to identify common reactions and their relationship to disease severity. Immunohistochemistry was used oil formalin-fixed, paraffin-embedded sections from the putamen, pons, and substantia nigra from 13 Parkinson disease (PD), 29 multiple-system atrophy (MSA), 34 progressive supranuclear palsy (PSP), 10 corticobasal degeneration (CBD), and 13 control cases. Classic reactive astrocytes were observed in MSA, PSP, and CBD, but not PD cases; the extent of reactivity correlated with indices of neurodegeneration and disease stage. Approximately 40% to 45% of subcortical astrocytes in PD and PSP accumulated alpha-synuclein and phospho-tall, respectively; subcortical astrocytes in MSA and CBD cases did not accumulate these proteins. Protoplasmic astrocytes were identified from fibrous astrocytes by their expression of parkin coregulated gene and apolipoprotein D, and accumulated abnormal proteins in PD, PSP and CBD, but not MSA. The increased reactivity of parkin coregulated gene-immunoreactive protoplasmic astrocytes correlated with parkin expression in PSP and CBD. Non-reactive protoplasmic astrocytes were observed in PD and MSA cases; in PD, they accumulated alpha-synuclein, suggesting that the attenuated response might be due to all increase in the level of alpha-synuclein. These heterogenous astroglial responses in PD, MSA, PSP, and CBD indicate distinct underlying pathogenic mechanisms in each disorder.

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