miR-342-5p decreases ankyrin G levels in Alzheimer's disease transgenic mouse models

Cell Rep. 2014 Jan 30;6(2):264-70. doi: 10.1016/j.celrep.2013.12.028. Epub 2014 Jan 16.

Abstract

MicroRNA alterations and axonopathy have been reported in patients with Alzheimer's disease (AD) and in AD mouse models. We now report that miR-342-5p is upregulated in APP/PS1, PS1ΔE9, and PS1-M146V transgenic AD mice, and that this upregulation is mechanistically linked to elevated β-catenin, c-Myc, and interferon regulatory factor-9. The increased miR-342-5p downregulates the expression of ankyrin G (AnkG), a protein that is known to play a critical role at the axon initial segment. Thus, a specific miRNA alteration may contribute to AD axonopathy by downregulating AnkG.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / genetics
  • Alzheimer Disease / metabolism*
  • Amyloid beta-Protein Precursor / genetics
  • Animals
  • Ankyrins / genetics
  • Ankyrins / metabolism*
  • Axons / metabolism
  • Cells, Cultured
  • Humans
  • Interferon-Stimulated Gene Factor 3, gamma Subunit / genetics
  • Interferon-Stimulated Gene Factor 3, gamma Subunit / metabolism
  • Mice
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Presenilin-1 / genetics
  • Proto-Oncogene Proteins c-myc / genetics
  • Proto-Oncogene Proteins c-myc / metabolism
  • beta Catenin / genetics
  • beta Catenin / metabolism

Substances

  • Amyloid beta-Protein Precursor
  • Ank3 protein, mouse
  • Ankyrins
  • Interferon-Stimulated Gene Factor 3, gamma Subunit
  • MicroRNAs
  • Mirn342 microRNA, mouse
  • Presenilin-1
  • Proto-Oncogene Proteins c-myc
  • beta Catenin