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  • Open Access

FcgRIIb mediates amyloid-β neurotoxicity and memory impairment in a model of Alzheimer’s disease

  • 1
Molecular Neurodegeneration20138 (Suppl 1) :P22

  • Published:


  • Memory Impairment
  • Primary Neuron
  • Neuronal Dysfunction
  • Synaptic Density
  • Genetic Depletion

Amyloid-β (Aβ) induces neuronal loss and cognitive deficits and is believed to be a prominent cause of Alzheimer’s disease (AD). However, the cellular mechanism of the pathogenesis is not fully understood. Here we report that Fcg-receptor IIb (FcgRIIb) mediates Aβ neurotoxicity and neurodegeneration. We found that FcgRIIb is significantly up-regulated in the hippocampus of AD brains and neuronal cells exposed to Aβ1-42. Neuronal FcgRIIb activates ER stress and caspase-12, and FcgRIIb knockout primary neurons are resistant to Aβ1-42-induced cell death in vitro. FcgRIIb deficiency ameliorates Aβ1-42-induced inhibition of long-term potentiation and inhibits the reduction of synaptic density by naturally secreted Aβ. Moreover, genetic depletion of FcgRIIb rescues the memory impairments in AD model mice. In an action mode of FcgRIIb in Aβ neurotoxicity, we found that soluble Aβ1-42 oligomers interact with FcgRIIb in vitro and in AD brains, and inhibition of their interaction blocks Aβ1-42 neurotoxicity. Thus, we conclude that FcgRIIb has an aberrant but essential role in Aβ1-42-mediated neuronal dysfunction, providing insight into Aβ neuropathology.

Authors’ Affiliations

School of Biological Sciences, Seoul, Republic of Korea


© Jung; licensee BioMed Central Ltd. 2013

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.