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Epigenetic Control of Somatostatin and Cortistatin Expression by Beta Amyloid Peptide

AuthorsRubio, Alicia; Sánchez-Mut, José V.; García, Esther; Velasquez, Zahady D.; Oliver de la Cruz, Jorge ; Esteller, Manel; Ávila, Jesús
Alzheimer’s disease
Histone methylation
Issue Date2011
PublisherJohn Wiley & Sons
CitationJournal of Neuroscience Research 90 (1): 13-20 (2011)
AbstractBeta 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
Publisher version (URL)http://dx.doi.org/10.1002/jnr.22731
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