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Interaction of NO with Cu and heme-bound Aβ peptides associated with Alzheimer's disease

Chandradeep Ghosh1, Debajyoti Pramanik, Soumya Mukherjee

  • 1Department of Inorganic Chemistry, Indian Association for the Cultivation of Science, Kolkata, India 700032.

Inorganic Chemistry
|December 11, 2012
PubMed

Insights

Nitric oxide (NO) reduces the toxicity of amyloid-beta (Aβ) peptides in Alzheimer's disease (AD) by altering copper (Cu) and heme binding. This interaction decreases harmful oxygen species and releases heme, suggesting a protective role for NO in AD.

Area of Science:

  • Biochemistry
  • Neuroscience
  • Spectroscopy

Background:

  • Copper (Cu) and heme are implicated in Alzheimer's disease (AD) pathogenesis.
  • Amyloid-beta (Aβ) peptides binding both Cu and heme generate toxic partially reduced oxygen species (PROS).
  • Reduced nitric oxide (NO) synthase activity is observed in AD patients.

Purpose of the Study:

  • Investigate the interaction of NO with Cu and heme-bound Aβ peptides.
  • Determine the effect of NO on the toxicity of these complexes.
  • Elucidate the mechanism of NO's action.

Main Methods:

  • Absorption spectroscopy
  • Electron Paramagnetic Resonance (EPR) spectroscopy
  • Resonance Raman spectroscopy
  • Kinetic assays

Main Results:

  • NO oxidizes Cu(I) sites in the Aβ complex, reducing PROS generation.
  • NO facilitates the release of heme from Aβ peptides.
  • A tyrosine-mediated electron transfer mechanism was identified between Cu and heme sites.

Conclusions:

  • NO ameliorates the toxic effects of Cu and heme binding to Aβ peptides in AD.
  • NO's interaction with Aβ-Cu-heme complexes offers a potential therapeutic pathway for AD.
  • The findings provide a mechanistic basis for NO's protective role in Alzheimer's disease.

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