• Alessandra Masala, Simona Sanna, Sonia Esposito, Mauro Rassu, Manuela Galioto, Angelo Zinellu, Ciriaco Carru, Maria Teresa Carrì, Ciro Iaccarino, and Claudia Crosio.
• Department of Biomedical Science, University of Sassari, Viale San Pietro 43, 07100 Sassari, Italy.
• Neuroscience. 2018 Oct 15; 390: 1-11.

AbstractNeurodegenerative disorders, including Amyotrophic Lateral Sclerosis (ALS), have been associated to alterations in chromatin structure resulting in long-lasting changes in gene expression. ALS is predominantly a sporadic disease and environmental triggers may be involved in its onset. In this respect, alterations in the epigenome can provide the key to transform the genetic information into phenotype. In this paper, we demonstrate that two modifications associated with transcriptional activation, namely dimethylation of lysine 4 on H3 tail (H3K4me2) and phospho-acetylation of serine 10 and lysine 14 on H3 tail (H3K14ac-S10ph), and two modifications associated to transcriptional repression, namely trimethylation of lysine 9 on H3 tail (H3K9me3) and DNA methylation are selectively altered in cellular and animal model of ALS. These results reinforce the idea that epigenetic therapy may represent a potential and attractive approach for ALS treatment.Copyright © 2018 IBRO. Published by Elsevier Ltd. All rights reserved.

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