In the brains of Alzheimer's disease (AD) patients the accumulation of amyloid-β (Aβ) is known to be associated with memory loss and neuronal degeneration, but the mechanism of Aβ pathogenesis is not fully understood.
In this issue of the Journal of Clinical Investigation
, researchers led by Yong-Keun Jung at Seoul National University demonstrate that Aβ binds to a cellular protein known as FCγRIIb. Greater levels of FCγRIIb were detected in the brains of AD patients.
Binding of Aβ to FCγRIIb activated cell stress and death pathways. In a mouse model of AD, depletion of FCγRIIb ameliorated memory impairment. This study demonstrates that FCγRIIb plays a critical role in AD pathogenesis.