Affiliations: [a] CAS Key Laboratory of Genome Sciences and Information, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing, China | [b] University of Chinese Academy of Sciences, Beijing, China | [c] MIND Institute, School of Medicine, University of California at Davis, Sacramento, CA, USA | [d] UC Davis Genome Center and Department of Biomedical Engineering, Davis, CA, USA
Correspondence:
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Correspondence to: Hongxing Lei, CAS Key Laboratory of Genome Sciences and Information, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing, 100101, China. Tel/Fax: +86 10 84097276; E-mail: leihx@big.ac.cn; and Yong Duan, UC Davis Genome Center and Department of Biomedical Engineering, One Shields Avenue, Davis, CA 95616, USA. Tel.: +1 530 754 7632; E-mail: duan@ucdavis.edu.
Note: [1] These authors contributed equally to this manuscript.
Abstract: Genetic studies have identified several genomic loci including chr19p13.2 relevant to Alzheimer's disease (AD) susceptibility. However, the functional roles of these genomic loci in AD pathogenesis require further clarification. Transcriptome as an endophenotype is critical for the understanding of disease mechanism. Here we demonstrate that chr19p is the most significantly perturbed chromosome region in AD brain transcriptome. With dual evidence from genome and transcriptome, chr19p likely play a special role in AD pathogenesis.
