CpG and nonCpG methylation patterns of PSEN1 during neurodevelopment and neurodegeneration in mice and humans.

27th February 2015
Versione stampabile

Messaggio di errore

An unexpected error occurred while connecting to the Alfresco repository. Please contact the server administrator for assistance.

Venue: Edificio Povo 2, via Sommarive nr. 9, Povo (TN) - Room B101
 at 2:30 p.m.

  • Andrea Fuso, Dept. of Psychology, Sapienza University of Rome and S. Lucia Foundation, Lab. of Lipid Neurochemistry

The work on Presenilin1 (PSEN1) genes started in early 2000 with the observation that expression of this gene, involved in Alzheimer’s Disease (AD), was modulated by DNA methylation. Working with a mouse model of AD (TgCRND8 mice) it was possible to demonstrate that nutritionally-induced impairment of methylation metabolism resulted in PSEN1 hypomethylation and overexpression, with consequent exacerbation of AD-like features in mice. Conversely, nutritional supplementation with a methyl-donor resulted in the maintaining of control-like phenotype. At the same time, studies on the basic methylation mechanisms pointed out relevant non-CpG methylation in the experimental models used. The recent participation to a EU FP7 project (DEVELAGE) allowed to profile the epigenetic regulation of PSEN1 (among other genes) in course of neurodevelopment and neurodegeneration, in the TgCRND8 model and in human brain samples. Moreover, extending the non-CpG studies in these samples, it was possible to further characterize the role of this modification and to disclose a technical bias in the technique commonly used for the assessment of DNA methylation.