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Title: Epigenetic control of somatostatin and cortistatin expression by β amyloid peptide. Author: Rubio A, Sánchez-Mut JV, García E, Velasquez ZD, Oliver J, Esteller M, Avila J. Journal: J Neurosci Res; 2012 Jan; 90(1):13-20. PubMed ID: 21922516. Abstract: 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.[Abstract] [Full Text] [Related] [New Search]