Nature Communications (Jun 2016)

Early synaptic deficits in the APP/PS1 mouse model of Alzheimer’s disease involve neuronal adenosine A2A receptors

  • Silvia Viana da Silva,
  • Matthias Georg Haberl,
  • Pei Zhang,
  • Philipp Bethge,
  • Cristina Lemos,
  • Nélio Gonçalves,
  • Adam Gorlewicz,
  • Meryl Malezieux,
  • Francisco Q. Gonçalves,
  • Noëlle Grosjean,
  • Christophe Blanchet,
  • Andreas Frick,
  • U Valentin Nägerl,
  • Rodrigo A. Cunha,
  • Christophe Mulle

DOI
https://doi.org/10.1038/ncomms11915
Journal volume & issue
Vol. 7, no. 1
pp. 1 – 11

Abstract

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Hippocampal synaptic dysfunctions are an early symptom of Alzheimer’s disease. Here, the authors find adenosine A2A receptors are up-regulated in APP/PS1 model mice and that deleting or blocking receptor activity helps alleviate plasticity and memory impairments.