DNA methylation map of mouse and human brain identifies target genes in Alzheimer’s disease

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DNA methylation map of mouse and human brain identifies target genes in Alzheimer’s disease

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Title: DNA methylation map of mouse and human brain identifies target genes in Alzheimer’s disease
Author: Sanchez-Mut, Jose V.; Aso, Ester; Panayotis, Nicolas; Lott, Ira; Dierssen, Mara; Rabano, Alberto; Urdinguio, Rocio G.; Fernandez, Agustin F.; Astudillo, Aurora; Martin-Subero, Jose I.; Balint, Balazs; Fraga, Mario F.; Gomez, Antonio; Gurnot, Cecile; Roux, Jean-Christophe; Avila, Jesus; Hensch, Takao K.; Ferrer, Isidre; Esteller, Manel

Note: Order does not necessarily reflect citation order of authors.

Citation: Sanchez-Mut, J. V., E. Aso, N. Panayotis, I. Lott, M. Dierssen, A. Rabano, R. G. Urdinguio, et al. 2013. “DNA methylation map of mouse and human brain identifies target genes in Alzheimer’s disease.” Brain 136 (10): 3018-3027. doi:10.1093/brain/awt237. http://dx.doi.org/10.1093/brain/awt237.
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Abstract: The central nervous system has a pattern of gene expression that is closely regulated with respect to functional and anatomical regions. DNA methylation is a major regulator of transcriptional activity, and aberrations in the distribution of this epigenetic mark may be involved in many neurological disorders, such as Alzheimer’s disease. Herein, we have analysed 12 distinct mouse brain regions according to their CpG 5’-end gene methylation patterns and observed their unique epigenetic landscapes. The DNA methylomes obtained from the cerebral cortex were used to identify aberrant DNA methylation changes that occurred in two mouse models of Alzheimer’s disease. We were able to translate these findings to patients with Alzheimer’s disease, identifying DNA methylation-associated silencing of three targets genes: thromboxane A2 receptor (TBXA2R), sorbin and SH3 domain containing 3 (SORBS3) and spectrin beta 4 (SPTBN4). These hypermethylation targets indicate that the cyclic AMP response element-binding protein (CREB) activation pathway and the axon initial segment could contribute to the disease.
Published Version: doi:10.1093/brain/awt237
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3784285/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:11878816
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