Tetrahydrocurcumin Confers Protection Against Amyloid β-induced Toxicity

Neuroreport. 2011 Jan 5;22(1):23-7. doi: 10.1097/WNR.0b013e328341e141.

Abstract

Amyloid plaques and neurofibrillary tangles are the hallmarks of Alzheimer's disease. Amyloid β, a primary component of the amyloid plaques, is neurotoxic. Considerable attention has been directed toward identifying compounds with neuroprotective properties. Using rat primary hippocampal cultures, we show that tetrahydrocurcumin (THC), a metabolite of curcumin, shows a protective effect against oligomeric amyloid-β-induced toxicity. We further show that THC reduces amyloid-β-induced (i) increase in the level of reactive oxygen species, (ii) decrease in mitochondrial membrane potential, and (iii) caspase activation. In addition, we show that THC protects human neurons from oligomeric amyloid-β-induced toxicity as well. Thus, THC confers protection against amyloid-β-induced toxicity, and the antioxidant activity may contribute to its protective effect.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amyloid beta-Peptides / toxicity*
  • Animals
  • Antioxidants / pharmacology
  • Curcumin / analogs & derivatives*
  • Curcumin / pharmacology
  • Hippocampus / drug effects*
  • Humans
  • In Situ Nick-End Labeling
  • Membrane Potential, Mitochondrial / drug effects
  • Neurons / drug effects*
  • Neuroprotective Agents / pharmacology*
  • Organ Culture Techniques
  • Rats
  • Rats, Sprague-Dawley
  • Reactive Oxygen Species / metabolism

Substances

  • Amyloid beta-Peptides
  • Antioxidants
  • Neuroprotective Agents
  • Reactive Oxygen Species
  • tetrahydrocurcumin
  • Curcumin