Microglial Cx3cr1 knockout prevents neuron loss in a mouse model of Alzheimer's disease

Nat Neurosci. 2010 Apr;13(4):411-3. doi: 10.1038/nn.2511. Epub 2010 Mar 21.

Abstract

Microglia, the immune cells of the brain, can have a beneficial effect in Alzheimer's disease by phagocytosing amyloid-beta. Two-photon in vivo imaging of neuron loss in the intact brain of living Alzheimer's disease mice revealed an involvement of microglia in neuron elimination, indicated by locally increased number and migration velocity of microglia around lost neurons. Knockout of the microglial chemokine receptor Cx3cr1, which is critical in neuron-microglia communication, prevented neuron loss.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / genetics
  • Alzheimer Disease / metabolism*
  • Alzheimer Disease / pathology
  • Animals
  • CX3C Chemokine Receptor 1
  • Cell Communication / genetics
  • Cell Count
  • Disease Models, Animal
  • Gene Knock-In Techniques
  • Mice
  • Mice, Knockout
  • Mice, Transgenic
  • Microglia / metabolism*
  • Microglia / pathology
  • Neurons / metabolism*
  • Neurons / pathology
  • Receptors, Chemokine / deficiency*
  • Receptors, Chemokine / genetics

Substances

  • CX3C Chemokine Receptor 1
  • Cx3cr1 protein, mouse
  • Receptors, Chemokine