Comparision of time-course gene expression in wild-type Drosophila and an Alzheimers disease model

The strongest risk factor for developing Alzheimer's Disease (AD) is age. Here, we study the relationship between ageing and AD using a systems biology approach that employs a Drosophila (fruitfly) model of AD in which the flies overexpress the human Aβ42 peptide. We identified 712 genes that are differentially expressed between control and Aβ-expressing flies. We further divided these genes according to how they change over the animal's lifetime and discovered that the AD-related gene expression signature is age- independent. We have identified a number of differentially expressed pathways that are likely to play an important role in the disease, including oxidative stress and innate immunity. In particular, we uncovered two new modifiers of the Aβ phenotype, namely Sod3 and PGRP-SC1b. Transcript level measured using microarrays in biological quadruplicate (except day 20 which is in biological triplicate), each array is Aβ vs control at the same timepoint (defined by % survival), one replicate per array with dye-swaps.