Many genetic studies have focused on finding candidate genes for neurological disorders. Typically, the genome is surveyed for genome variation that is over represented within a collection of people at risk for disease; however, the biology behind most of these changes is elusive at best. one study found that many of the genetic variants that are replicated and known to be over-represented in Alzheimer’s disease do not change the sequence of the corresponding protein and thus the downstream effects of these risk variants are unknown  ( Our lab has focussed on trying to find additional genetic risk factors for Alzheimer’s disease as well as determining their immediate downstream effects. We hypothesize that one of the most likely downstream effects of non-coding variation is to change the expression of transcripts (Hardy and Myers, 2007). we have a series of human brain tissues from Alzheimer’s disease and control samples where we have looked at genome-wide DNA variation as well as transcriptome-wide RNA expression. Further studies in collaboration with the Pacific Northwest National Laboratories ( are now performing lc-ms experiments to capture proteome changes as well.