Aβ(1-42)-induced JNK and ERK activation in rabbit hippocampus is differentially regulated by lithium but is not involved in the phosphorylation of tau

Othman Ghribi, Patcharin Prammonjago, Mary M. Herman, Natalie K. Spaulding, John Savory

Research output: Contribution to journalArticle

33 Scopus citations

Abstract

Administration of Aβ(1-42) into the rabbit brain induces apoptosis and phosphorylation of tau. These Aβ effects correlate with the activation of JNK and ERK, but not of p38. Treatment with 7 mM lithium inhibits apoptosis, modulates JNK and ERK and does not affect the phosphorylation of tau. Our results demonstrate that lithium, at this dose, effectively inhibits the Aβ-induced apoptosis but has no effect on tau phosphorylation, and that MAP kinases are not involved in the phosphorylation of tau.

Original languageEnglish (US)
Pages (from-to)201-206
Number of pages6
JournalMolecular Brain Research
Volume119
Issue number2
DOIs
StatePublished - Nov 26 2003

Keywords

  • Caspase-3
  • ERK
  • JNK
  • Lithium
  • tau

ASJC Scopus subject areas

  • Molecular Biology
  • Cellular and Molecular Neuroscience

Fingerprint Dive into the research topics of 'Aβ(1-42)-induced JNK and ERK activation in rabbit hippocampus is differentially regulated by lithium but is not involved in the phosphorylation of tau'. Together they form a unique fingerprint.

  • Cite this