Protective effect of caffeic acid against beta-amyloid-induced neurotoxicity by the inhibition of calcium influx and tau phosphorylation

Dong Geun Sul, Hyo Shin Kim, Dongho Lee, Seong Soo Joo, Kwang Woo Hwang, So Young Park

Research output: Contribution to journalArticle

101 Citations (Scopus)


Aims: The progressive accumulation of beta-amyloid peptide (Aβ), in the form of senile plaques, has been recognized as one of the major causes of Alzheimer's disease (AD) pathology. Increased production of Aβ and the aggregation of Aβ to oligomers have been reported to trigger neurotoxicity, oxidative damage and inflammation. Furthermore, Aβ-induced tau hyperphosphorylation and neurotoxicity are downstream of Aβ. Therefore, we studied the possible neuroprotective effects of caffeic acid against Aβ-induced toxicity. Main methods: Treatment of PC12 cells with 10 μM Aβ (25-35) for 24 h significantly decreased the cell viability; this was accompanied by an increase in intracellular calcium levels and tau phosphorylation with GSK-3β (glycogen synthase kinase-3β) activation (phosphorylation). Key findings: However, pretreatment of the PC12 cells with 10 and 20 μg/ml of caffeic acid, for 1 h prior to Aβ, significantly reversed the Aβ-induced neurotoxicity by attenuating the elevation of intracellular calcium levels and tau phosphorylation. Significance: Taken together, these results suggest that caffeic acid protected the PC12 cells against Aβ-induced toxicity. In addition, the neuroprotective mechanisms of caffeic acid against Aβ attenuated intracellular calcium influx and decreased tau phosphorylation by the reduction of GSK-3β activation.

Original languageEnglish
Pages (from-to)257-262
Number of pages6
JournalLife Sciences
Issue number9-10
Publication statusPublished - 2009 Feb 27



  • Antioxidant
  • Beta-amyloid
  • Caffeic acid
  • Calcium influx
  • GSK-3β
  • Tau phosphorylation

ASJC Scopus subject areas

  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Biochemistry, Genetics and Molecular Biology(all)

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