A 2015 article, Integrated genomic approaches identify major pathways and upstream regulators in late onset Alzheimer's disease, provides complicated science that could get lost if we don't pause and try and understand.
Certain mutations in APP, PSEN1 and PSEN2 inevitably lead to early-onset AD (EOAD) at around the age of 50 years in five percent of sufferers. Approximately 50% of the risk of late onset AD (LOAD) can be explained by genetic factors. The apolipoprotein E variant, APOE4, found in 15% of the population, is the major genetic risk factor for LOAD. APOE4 contributes around six percent to the phenotypic variance in AD, and it is estimated that between 40% and 65% of people diagnosed with AD have one or two copies of the variant APOE4 gene--Nature Publishing Group
Gene set enrichment analysis (GSEA) for NOROS.GSEA confirms that the NOROS gene set containing up-regulated LOAD DEGs is enriched in old people. Microarray data for aging (GSE53890) were analysed using GSEA software to identify significant gene sets (see Methods). The enrichment plot on the left shows the distribution of genes in the set that are correlated with the old or young phenotype. The heatmap on the right shows where gene expression is relatively high (red) or low (blue) for each gene in the indicated sample.
The exciting part about attending the White House Conference on Aging? The ability to measure change and progress in the development of social programs that support our aging society. The conference is held every ten years so there are a lot of successes as well as requested needed interventions to address persistent gaps. I will be traveling the next few weeks to attend a few conferences--2015 National Conference on Health Statistics, Preventing Overdiagnosis meeting being held at the National Institutes of Health and INBOUND 2015, advances in creating a brand that resonates and provides value. Thank you for supporting, Alzheimer's Disease: The Brand. (@alzheimersbrand)