Rubio_2012_J.Neurosci.Res_90_13

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