The increase in life expectancy in Western countries has brought to the surface, among other things, an increase in diagnosed cases of neurodegenerative diseases such as dementia would. We know very little about the cellular and molecular basis of these, and even fewer have treatments with a real impact on the course of the disease. The best known is Alzheimer’s disease, but other relevant dementias in our area are also associated with Lewy bodies, that linked to Parkinson’s disease and which could develop long-term Down syndrome. It is interesting to recognize that they all have similar characteristics under the microscope, with some overlap in the clinical symptoms, so you might think that there is a shared biological basis for all of them. Today, an article published in the Translational Psychiatry Journal (Nature group), Manel Esteller, director of the Epigenetics and Cancer Biology Program (PEBC) of the Bellvitge Institute for Biomedical Research (IDIBELL) and ICREA researcher professor of Genetics at the University of Barcelona, shows that all mentioned dementias possess a common group of chemically inactivated genes. This demonstrates the existence of a single initial trunk for the disease.

“We have analyzed the chemical marks that determine the activity of the genome, called the epigenome, of the gray matter from 75 patients with various dementias and have found that these people share an erroneous off or on of a common set of 20 genes.” —Says Dr . Manel Esteller— “and what it is even more exciting is that some of them were also found by other groups independently, and this indicates that these genes could be truly involved in the development of Alzheimer’s and dementia in general. Among these they include ankyrin-1, involved in contacts between cells and RHOM2 related to inflammatory processes.” —Dr Esteller explains, and concludes about his research— “Now, it will be important to begin studying whether these altered genes can be targets for drugs that are so necessary today for these increasing frequency diseases for which we have very few treatment options.”

Article: Sanchez-Mut JV, Heyn H, Vidal E, Moran S, Sayols S, Delgado-Morales R, Schultz MD, Ansoleaga B, Garcia-Esparcia P, Pons-Espinal M, Martinez de Lagran M, Dopazo J, Rabano A, Avila J, Dierssen M, Lott I, Ferrer I, Ecker JR, Esteller M. Human DNA methylomes of neurodegenerative diseases show common epigenomic patterns.