Epigenetic control of somatostatin and cortistatin expression by β amyloid peptide.

Rubio A, Sánchez-Mut JV, García E, Velasquez ZD, Oliver J, Esteller M, Avila J

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.

LowCell ChIP kit

Share this article

January, 2012



 See all events


 See all news

The European Regional Development Fund and Wallonia are investing in your future.

Extension of industrial buildings and new laboratories.


       Site map   |   Contact us   |   Conditions of sales   |   Conditions of purchase   |   Privacy policy   |   Diagenode Diagnostics