. FcγRIIb mediates amyloid-β neurotoxicity and memory impairment in Alzheimer's disease. J Clin Invest. 2013 Jul 1;123(7):2791-802. PubMed.


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  1. This is an interesting study showing that primary cortical neurons exposed to synthetic Aβ42 oligomers upregulated FcγRIIb via JNK signaling. Did the authors see any effect of Aβ40 oligomers on this particular receptor? So far authors have used J20; is it possible to see the same effect in other Alzheimer's transgenic mice?

    View all comments by Suhail Rasool
  2. This is a very interesting finding that directly correlates with our work at Crossbeta. For studying the effect of compounds on the interaction between Aβ oligomers and a receptor present on neurons and inflammatory cells, we have successfully developed a biochemical high-throughput screening assay on the basis of Perkin Elmer's AlphaScreen technology for studying molecular interactions. The Aβ oligomers that we applied in this screening assay have been stabilized and purified to avoid interference by monomeric Aβ and fibrils and thus improve statistical power while maintaining functionality of the oligomers.

    Using this assay, we performed an HTS campaign to identify small molecules that inhibit the oligomer-receptor interactions. For follow-up we have selected the compounds that specifically bind to the oligomers and not to the receptor, thus avoiding side effects due to blocking the physiological function of the receptor. The screening platform we developed at Crossbeta could be adapted to FcγRIIb, and we would welcome a discussion. Our stabilized oligomers could also be evaluated upon request.

    View all comments by Armand Tepper

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  1. Immune Cell Receptor Gives Aβ a Toxic Edge