中文
Published date:2013-09-25    Provided by:
Guest Speaker: 雷红星 博士(中国科学院北京基因组研究所任研究员)

Time:

2012-05-17  14:30

Location School of Science Meeting Room
Content: 

.The dominant theory regarding the pathogenesis of Alzheimer’s disease (AD) has been amyloid cascade hypothesis. However, clinical trials targeting amyloid clearance and Abeta production have thus far been very disappointing. Therefore, pursuing alternative strategies becomes an imminent task. Systems biology approach can be used to generate hypothesis based on the genomic, transcriptomic and other omics data. Over the last decade, microarray studies on the brain transcriptome of AD patients have accumulated rich information. We have analyzed all publically available data using the same analytical procedure in order to look for common mechanism. An interesting observation is the down-regulation of energy metabolism at the early stage in the absence of enhanced signal transduction. This is unlikely caused by the damage to mitochondrion due to oxidative stress. Rather, we propose that the down-regulation of energy metabolism is a protective response of neurons to the microenvironment with poor energy supply. We have described this adaptation strategy with gene and pathway level details in our recent works.

Date Modified:2012-05-17