Clustering of transcriptional profiles identifies changes to insulin signaling as an early event in a mouse model of Alzheimer's disease

BMC Genomics. 2013 Nov 25:14:831. doi: 10.1186/1471-2164-14-831.

Abstract

Background: Alzheimer's disease affects more than 35 million people worldwide but there is no known cure. Age is the strongest risk factor for Alzheimer's disease but it is not clear how age-related changes impact the disease. Here, we used a mouse model of Alzheimer's disease to identify age-specific changes that occur prior to and at the onset of traditional Alzheimer-related phenotypes including amyloid plaque formation. To identify these early events we used transcriptional profiling of mouse brains combined with computational approaches including singular value decomposition and hierarchical clustering.

Results: Our study identifies three key events in early stages of Alzheimer's disease. First, the most important drivers of Alzheimer's disease onset in these mice are age-specific changes. These include perturbations of the ribosome and oxidative phosphorylation pathways. Second, the earliest detectable disease-specific changes occur to genes commonly associated with the hypothalamic-adrenal-pituitary (HPA) axis. These include the down-regulation of genes relating to metabolism, depression and appetite. Finally, insulin signaling, in particular the down-regulation of the insulin receptor substrate 4 (Irs4) gene, may be an important event in the transition from age-related changes to Alzheimer's disease specific-changes.

Conclusion: A combination of transcriptional profiling combined with computational analyses has uncovered novel features relevant to Alzheimer's disease in a widely used mouse model and offers avenues for further exploration into early stages of AD.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / genetics
  • Alzheimer Disease / metabolism*
  • Animals
  • Cerebral Cortex / metabolism
  • Cluster Analysis
  • Disease Models, Animal
  • Female
  • Humans
  • Hypothalamo-Hypophyseal System / metabolism
  • Insulin / physiology
  • Insulin Receptor Substrate Proteins / metabolism*
  • Mice
  • Mice, Inbred C57BL
  • Oxytocin / metabolism
  • Phenotype
  • Pituitary-Adrenal System / metabolism
  • Signal Transduction
  • Transcription, Genetic
  • Transcriptome*

Substances

  • Insulin
  • Insulin Receptor Substrate Proteins
  • Irs4 protein, mouse
  • Oxytocin