Epigenetic control of somatostatin and cortistatin expression by β amyloid peptide

Alicia Rubio, José V. Sánchez-Mut, Esther García, Zahady D. Velasquez, Jorge Oliver, Manel Esteller, Jesús Avila

Research output: Contribution to journalArticlepeer-review


β Amyloid, present in senile plaques, has been related largely to neuronal loss in the brain of patients with Alzheimer's disease. However, how neurons respond to β amyloid insults is still poorly understood. Here we show that β amyloid increases somatostatin and cortistatin gene expression mainly through an increase in histone 3 lysine 4 methylation (H3K4me3), a modification associated with transcriptional activation. Somatostatin and cortistatin partially decreased β amyloid toxicity in primary cortical neurons in culture. Thus we suggest that neurons respond to β amyloid insults by releasing somatostatin and cortistatin, which will act as a protective agent against β amyloid toxicity. Our results suggest a relevant function for both neuropeptides against β amyloid toxicity, providing new insights into Alzheimer's disease.

Original languageEnglish
Pages (from-to)13-20
Number of pages8
JournalJournal of Neuroscience Research
Issue number1
Publication statusPublished - Jan 2012


  • Alzheimer's disease
  • GSK3
  • Histone methylation

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

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