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Cell death mechanisms in multiple system atrophy

S Probst-Cousin1, C H Rickert, K W Schmid

  • 1Centre of Neuromuscular Disorders, Department of Neurology, Friedrich-Alexander-University, Erlangen-Nuremberg, Erlangen, Germany.

Journal of Neuropathology and Experimental Neurology
|September 16, 1998
PubMed
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Multiple system atrophy (MSA) primarily involves oligodendrocyte apoptosis, distinguishing it from other neurodegenerative diseases. This cellular death pathway is central to MSA pathogenesis.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathology

Background:

  • Multiple system atrophy (MSA) is a neurodegenerative disorder characterized by progressive autonomic failure and parkinsonism.
  • The precise mechanisms driving neuronal loss in MSA remain incompletely understood, necessitating further investigation into cell death pathways.

Purpose of the Study:

  • To investigate the presence and distribution of apoptotic cell death in oligodendrocytes and neurons in MSA.
  • To compare the distribution of apoptosis with glial cytoplasmic inclusions and the expression of key apoptosis-related proteins.

Main Methods:

  • Modified terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) for detecting apoptotic cells.
  • Immunohistochemistry to assess glial cytoplasmic inclusions, bcl-2, bax, CD95, TNFalpha, and p53 protein expression, and activated microglia.

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Main Results:

  • Apoptosis was predominantly observed in oligodendrocytes in MSA, correlating with known oligodendroglial pathology.
  • Upregulation of bcl-2 protein and coexpression with ubiquitin were noted in some glial cytoplasmic inclusions, suggesting an attempt to inhibit apoptosis.
  • Bax protein was detected in oligodendrocytes, and significant neuronal apoptosis was not observed, with neurons potentially undergoing secondary necrosis.

Conclusions:

  • Oligodendroglial apoptosis is a central pathological feature of multiple system atrophy.
  • The distinct pattern of oligodendroglial pathology in MSA differentiates it from other neurodegenerative diseases.