The Bjornsson et al. study provides further evidence that DNA methylation differences between individuals increase with age. However, the study not only confirms this principle, but shows that genetic factors play a role in inter-individual methylation differences. It highlights the complexities when studying DNA methylation in aging. While it is thought that "environmental" factors such as alcohol, diet, perhaps medications, etc., play a role in modifying DNA methylation patterns in the genome, genetic factors could play a role as well. Recently, we identified in a postmortem brain study 2/50 gene loci that showed significant alterations in Alzheimer's subjects, as compared to controls (Siegmund et al., 2007). Interestingly, the changes in the Alzheimer's cohort, in terms of DNA methylation, appeared to reflect an acceleration of normal aging. Therefore, one could assume that the findings of Bjornsson et al. will be of great interest for aging-related disorders, including Alzheimer disease.

View all comments by Schahram Akbarian

These are indeed highly interesting papers.

To add to the story of epigenetic influences in the aging process, a new and fascinating study was published in PLoS ONE. The group around Axel Schumacher et al. at the Technical University Munich/Germany could show that people with late-onset Alzheimer disease have indeed an increased “epigenetic drift” in genes that may be responsible for some of the observed phenotypes. Additionally, the group found that some genes that participate in amyloid-β processing and methylation homeostasis show a significant interindividual epigenetic variability, which may contribute to disease predisposition. The observed epigenetic pattern would complement and support the aforementioned data, showing that the changes in the Alzheimer brain appeared to reflect an acceleration of normal aging. This could indicate that everybody has a certain likelihood of developing the disease.

References:
Wang SC, Oelze B, Schumacher A. Age-specific epigenetic drift in late-onset Alzheimer's disease. PLoS ONE. 2008;3(7):e2698. Abstract

View all comments by Jutta Bremer