Soluble alpha-APP (sAPPalpha) regulates CDK5 expression and activity in neurons

PLoS One. 2013 Jun 11;8(6):e65920. doi: 10.1371/journal.pone.0065920. Print 2013.

Abstract

A growing body of evidence suggests a role for soluble alpha-amyloid precursor protein (sAPPalpha) in pathomechanisms of Alzheimer disease (AD). This cleavage product of APP was identified to have neurotrophic properties. However, it remained enigmatic what proteins, targeted by sAPPalpha, might be involved in such neuroprotective actions. Here, we used high-resolution two-dimensional polyacrylamide gel electrophoresis to analyze proteome changes downstream of sAPPalpha in neurons. We present evidence that sAPPalpha regulates expression and activity of CDK5, a kinase that plays an important role in AD pathology. We also identified the cytoprotective chaperone ORP150 to be induced by sAPPalpha as part of this protective response. Finally, we present functional evidence that the sAPPalpha receptor SORLA is essential to mediate such molecular functions of sAPPalpha in neurons.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amyloid beta-Protein Precursor / pharmacology*
  • Animals
  • Cells, Cultured
  • Cyclin-Dependent Kinase 5 / metabolism*
  • Electrophoresis, Gel, Two-Dimensional
  • Mass Spectrometry
  • Mice
  • Mice, Inbred BALB C
  • Neurons / drug effects*
  • Neurons / metabolism*

Substances

  • Amyloid beta-Protein Precursor
  • Cyclin-Dependent Kinase 5

Grants and funding

Studies were funded by grants from the American Health Assistance Foundation (to MR; www.brightfocus.org; project A2011601) and the German Research Foundation (to DH; www.dfg.de; project HA6155/2-2). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.