Glycoxidation and oxidative stress in Parkinson disease and diffuse Lewy body disease

R. Castellani*, M. A. Smith, P. L. Richey, G. Perry

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

289 Scopus citations


Oxidative stress is well accepted as an important pathogenic factor in Parkinson disease, based largely on indirect evidence. Recently, we have developed antibodies that recognize specific advanced glycation end-products (anti-pentosidine and anti-pyrraline), protein modifications that are potentiated by oxidative stress in a process termed glycoxidation. We applied these antibodies immunocytochemically to affected regions in Parkinson disease and diffuse Lewy body disease brains. Additionally, we used antibodies to heme oxygenase-1, a putative marker of oxidative stress response. Immunoreactivity to pentosidine, pyrraline, and heme oxygenase-1 was seen in the substantia nigra of Parkinson disease and the neocortex of diffuse Lewy body disease. Heme oxygenase-1 was further demonstrated by immunoelectron microscopy in intimate association with filaments of cortical Lewy bodies. Immunolocalization of advanced glycation end-products and a marker of oxidative stress response induction provides evidence that glycoxidation and oxidative stress may be an important pathogenic factor in diseases characterized by Lewy body formation, and furthers the evidence that cytoskeletal proteins and their inclusions are susceptible to oxidative stress.

Original languageEnglish (US)
Pages (from-to)195-200
Number of pages6
JournalBrain research
Issue number1-2
StatePublished - Oct 21 1996


  • Advanced glycation end-product
  • Diffuse Lewy body disease
  • Immunocytochemistry
  • Oxidative stress
  • Parkinson's disease

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology


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