Transcriptomics

Dataset Information

7

Transcription profiling by array of mouse hippocampus from APP-PS1 and wild-type male littermates treated with vehicle or ibuprofen from 3 to 6 months of age


ABSTRACT: NSAIDs (non-steroidal anti-inflammatory drugs) inhibit cyclooxygenase (COX) enzymes and prevent Alzheimer's disease (AD) at preclinical stages in cognitively normal aging populations. We modeled NSAID prevention of memory impairment in AD model mice to identify novel targets of NSAID action. We found that the widely-used NSAID ibuprofen prevented early hippocampus-dependent memory deficits in APP-PS1 mice. We therefore analyzed gene expression in the hippocampus of these mice. We treated male APPSwe-PS1deltaE9 mice (strain originally provided by Dr. David Borchelt and fully back-crossed to a C57BL/6J background) and their wild-type littermates with ibuprofen in chow from 3 to 6 months of age, after which we sacrificed the mice and dissected one hippocampus from each mouse for RNA isolation and microarray analysis. In each genotype-treatment group, we analyzed samples from 5 mice. Note: In our initial analysis, we found that sample GSM1644138, Hippocampus_WT_Con_rep5, was an outlier in overall gene expression. We therefore removed this sample before performing the analysis published in PMID 27190010.

REANALYSED by: E-GEOD-67306

ORGANISM(S): Mus musculus  

SUBMITTER: Nathaniel S Woodling   Katrin Andreasson  Katrin I Andreasson 

PROVIDER: E-GEOD-67306 | ArrayExpress | 2016-06-14

SECONDARY ACCESSION(S): GSE67306PRJNA279470

REPOSITORIES: GEO, ArrayExpress

Dataset's files

Source:
Action DRS
E-GEOD-67306.idf.txt Idf
E-GEOD-67306.processed.1.zip Processed
E-GEOD-67306.raw.1.zip Raw
E-GEOD-67306.sdrf.txt Txt
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Publications


Identifying preventive targets for Alzheimer's disease is a central challenge of modern medicine. Non-steroidal anti-inflammatory drugs, which inhibit the cyclooxygenase enzymes COX-1 and COX-2, reduce the risk of developing Alzheimer's disease in normal ageing populations. This preventive effect coincides with an extended preclinical phase that spans years to decades before onset of cognitive decline. In the brain, COX-2 is induced in neurons in response to excitatory synaptic activity and in g  ...[more]

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