This cover-story in Nucleic Acids Research received extensive world-wide feedback and was one of the most downloaded NAR papers in 2006.
Schumacher lab on the road:
Read about our study on epigenetics of late-onset Alzheimer's disease:
Have a look at our study of epigenetic changes in schizophrenia and bipolar disorder:
This study provides evidence of silencing of genes responsible for communication with the brain, brain development and other processes linked to schizophrenia and bipolar disorder.
This report was covered in several news stories around the world.
This database contains data derived from high-density chr. 21 and 22 Affymetrix tiling arrays consisting of over 340.000 oligonucleotide probe pairs in eight individuals (see Schumacher et al., 2006. Nucleic Acids Research). Tissue: Prefontal cortex. Measured is the hypomethylation, depicted as peaks.
The data is browsable via the USCS genome browser. This data is mirrored from the www.epigenomics.ca website.
This database contains data derived from whole genome, CpG island microarrays. Tissue: Male germ-cells. The objective of this study (see Flanagan et al., 2006. American Journal of Human Genetics) was to perform a comprehensive analysis of DNA methylation variation between and within the germlines of normal males. The microarray analysis has identified numerous DNA methylation-variable positions in the germ cell genome. The largest degree of variation was detected within the promoter CpG islands and pericentromeric satellites among the single-copy DNA fragments and repetitive elements, respectively.
The data is browsable via the USCS genome browser. This data is mirrored from the www.epigenomics.ca website.
This database contains data derived mass spectrophotometry analyses of post-mortem brain samples of late-onset Alzheimer's disease patients and controls (supplement to Wang et al., 2008).
Using MALDI-TOF mass spectrometry in post-mortem brain samples and lymphocytes, we have performed an analysis of DNA methylation across 12 potential Alzheimer's susceptibility loci. In the LOAD brain samples we identified a notably age-specific epigenetic drift, supporting a potential role of epigenetic effects in the development of the disease. Additionally, we found that some genes that participate in amyloid- processing (PSEN1, APOE) and methylation homeostasis (MTHFR, DNMT1) show a significant interindividual epigenetic variability, which may contribute to LOAD predisposition. The APOE gene was found to be of bimodal structure, with a hypomethylated CpG-poor promoter and a fully methylated 3'-CpG-island, that contains the sequences for the 4-haplotype, which is the only undisputed genetic risk factor for LOAD. Aberrant epigenetic control in this CpG-island may contribute to LOAD pathology.
