Epigenetic Control of Somatostatin and Cortistatin Expression by Beta Amyloid Peptide

Abstract

Beta 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 b amyloid insults is still poorly understood. Here we show that b 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 b amyloid toxicity in primary cortical neurons in culture. Thus we suggest that neurons respond to b amyloid insults by releasing somatostatin and cortistatin, which will act as a protective agent against b amyloid toxicity. Our results suggest a relevant function for both neuropeptides against b amyloid toxicity, providing new insights into Alzheimer’s disease