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Novel Phenoselenazines as Amyloid-β Aggregation Inhibitors.

Ahmed A Hefny1,2, Kartar Singh1, Rahul C Karuturi1

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Novel N-benzylphenoselenazine compounds show promise in inhibiting amyloid-beta (Aβ42) aggregation, a key factor in Alzheimer's disease. These compounds also possess antioxidant and disaggregation properties, offering a potential therapeutic strategy.

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Area of Science:

  • Medicinal Chemistry
  • Neuroscience
  • Biochemistry

Background:

  • Amyloid-beta (Aβ42) aggregation is a central pathological hallmark of Alzheimer's disease.
  • Developing effective inhibitors of Aβ42 aggregation is crucial for therapeutic intervention.

Purpose of the Study:

  • To design, synthesize, and evaluate novel N-benzylphenoselenazine derivatives as inhibitors of Aβ42 aggregation.
  • To assess the disaggregation and antioxidant properties of these compounds.
  • To investigate their potential in reducing Aβ42-mediated cytotoxicity.

Main Methods:

  • Synthesis of N-benzylphenoselenazine derivatives.
  • Thioflavin T-based fluorescence assay to monitor Aβ42 aggregation kinetics.
  • Cell-based assays to evaluate cytotoxicity.
  • Computational modeling to understand the mechanism of interaction.

Main Results:

  • Compounds 8i and 8j demonstrated significant inhibition of Aβ42 aggregation (∼91%), comparable to resveratrol and methylene blue.
  • Both compounds exhibited Aβ42 disaggregation (up to 76%) and antioxidant activity (up to 80.5%).
  • Compounds 8i and 8j reduced Aβ42-mediated cytotoxicity in cell culture.
  • Computational studies indicated interaction within the Aβ42 pentamer channel, stabilizing the assembly.

Conclusions:

  • N-benzylphenoselenazine derivatives are effective inhibitors of Aβ42 aggregation.
  • These compounds display multifaceted therapeutic potential, including disaggregation and antioxidant effects.
  • N-benzylphenoselenazines represent promising candidates for targeting the amyloid cascade in Alzheimer's disease therapy.