Antioxidant activity of X-34 in synaptosomal and neuronal systems

Jaroslaw Kanski, Rukhsana Sultana, William Klunk, D. Allan Butterfield

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


Inhibiting aggregation and deposition of amyloid β-peptide (Aβ) in brain is a therapeutic strategy for Alzheimer's disease (AD). A Congo-red-like molecule, X-34, is reported to bind to Aβ deposits. Oxidative stress associated with Aβ is hypothesized to be critical for the neurotoxic properties of this peptide. The present study was undertaken to test the hypothesis that X-34, with its salicylate groups, would act as an antioxidant. When challenged by hydroxyl or peroxyl free radicals or Aβ(1-42), oxidative stress and neurotoxicity occurred in neural systems as assessed by several indices. However, pretreatment of synaptosomes and primary neuronal cell culture with X-34 greatly ameliorated lipid peroxidation induced by these free radicals and Aβ(1-42). Protein oxidation was not prevented by X-34. These results are discussed in terms of potential therapeutic use of X-34 and related compounds in AD.

Original languageEnglish
Pages (from-to)173-179
Number of pages7
JournalBrain Research
Issue number1-2
StatePublished - Oct 24 2003

Bibliographical note

Funding Information:
This work was supported in part by NIH grants (AG-10836; AG-05119).


  • Amyloid β-peptide
  • Fibril
  • Free radical antioxidant
  • Oxidative stress
  • X-34

ASJC Scopus subject areas

  • General Neuroscience
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology


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