E-MTAB-4611 - Transcription profiling of Drosophila expressing mutant Abeta under treatment with lithium

Submitted on 8 February 2012, last updated on 26 January 2017, released on 26 January 2017
Drosophila melanogaster
Samples (14)
Array (1)
Protocols (5)
Our previous work in a Drosophila model of Alzheimer's disease (AD) has shown that we can intervene into the pathways to slow or prevent AD progression. Lithium was able to rescue toxicity in the Drosophila AD model which corresponded with a reduction in Abeta levels. Furthermore, we have demonstrated that Lithium affects Abeta protein translation. To this end, we were interested in studying the effect of Lithium on Abeta using microarray analyses, to determine if we could uncover any interesting downstream pathways. Flies were expressing a mutant version of Abeta, the Arctic mutation, which increases the aggregation or production of Abeta (UAS-ArcAb42/+;elavGS/+). We collected flies 2 days post eclosion that either had no Arctic Abeta protein, or expressed Arctic with or without Lithium treatment for 17 days post eclosion. Samples were homogenised using RLT buffer with betamercaptoethanol.
Experiment types
transcription profiling by array, case control design, compound treatment design, genetic modification design
Direct Keap1-Nrf2 disruption as a potential therapeutic target for Alzheimer’s disease. Fiona Kerr, Oyinkan Sofola-Adesakin, Dobril K. Ivanov, Beatriz Gomez Perez-Nievas, Helene C. Bertrand, Pedro Martinez, Rebecca Callard, Inge Snoeren, Helena M. Cocheme, Jennifer Adcott, Mobina Khericha, Jorge Ivan Castillo-Quan, Geoffrey Wells, Wendy Noble, Janet Thornton, Linda Partridge.
Investigation descriptionE-MTAB-4611.idf.txt
Sample and data relationshipE-MTAB-4611.sdrf.txt
Raw data (1)E-MTAB-4611.raw.1.zip
Array designA-AFFY-35.adf.txt