作者: David A. Bennett , Lei Yu , Jingyun Yang , Gyan P. Srivastava , Cristin Aubin
DOI: 10.1016/J.TRSL.2014.05.006
关键词: Epigenomics 、 Cognitive decline 、 Alzheimer's disease 、 PSEN2 、 Epigenome 、 Dementia 、 Biology 、 Genetics 、 SORL1 、 PSEN1
摘要: Alzheimer's disease (AD) is a large and growing public health problem. It characterized by the accumulation of amyloid β peptides abnormally phosphorylated tau proteins that are associated with cognitive decline dementia. Much has been learned about genomics AD from linkage analyses and, more recently, genome-wide association studies. Several but not all aspects genomic landscape involved in metabolism. The moderate concordance among twins suggests other factors, potentially epigenomic related to AD. We at earliest stages examining relation epigenome clinical pathologic phenotypes characterize Our literature review there some evidence age-related changes human brain methylation. Unfortunately, studies have relatively small limited coverage methylation sites microRNA, let alone marks. midst 2 brains including than 420,000 autosomal cytosine-guanine dinucleotides Illumina Infinium HumanMethylation450 BeadArray, histone acetylation chromatin immunoprecipitation sequencing. present descriptive data help inform researchers what expect these approaches better design power their then discuss future directions on architecture