In “Epigenetic changes in Alzheimer’s Disease: Decrements in DNA Methylation,” the authors investigate the loss of DNA methylation as a potential cause of the expression differences of genes in Alzheimer’s disease. Epigenetic mechanisms, such as DNA methylation, have the ability to affect the expression of a large numbers of genes, making them a possible cause of the expression differences found in Alzheimer’s disease. In this study, the authors observe the levels of DNA methylation and of proteins that support regular epigenetic function in the neurons of subjects with Alzheimer’s Disease and without. For the experiment, the Mastroeni et al. (2010) harvested brain samples of subjects both with and without Alzheimer’s disease quickly after death. The samples were then each washed with a different antibody solution that would reveal epigenetic mechanisms. The samples were observed and photographed under a microscope. The results showed striking differences in the levels of epigenetic mechanisms between the neurons of patients with Alzheimer’s and without as well as between different parts of the brain. The neurons of patients with Alzheimer’s disease exhibited significant decreases in methylation levels and decreases in proteins that form the MeCP1/MBD2 methylation complex, which helps to create and stabilize methylation sites. There was also an observed decrease of other methylation stabilization proteins, including stabilization proteins that affect ribosome production. This loss of methylation was specific to the entorhinal cortex, a part of the brain most susceptible to Alzheimer’s disease. The authors believe that these significant decreases in methylation levels in the neurons of subjects with Alzheimer’s Disease can provide an explanation for the abnormal function of a large number of genes found in Alzheimer’s disease. With further investigation, these findings may help provide answers about the pathogenesis of Alzheimer’s Disease.