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Amyloid-β oligomers (AβOs) impair presynaptic organization by reducing β-NRXs on the axon surface. AβOs bind to the histidine-rich domain (HRD) of β-NRXs. This interaction leads to the reduction of β-NRX surface expression on the axons without interfering with its ability to bind to NLGN1 or LRRTM2. By reducing the surface level of β-NRXs, presumably through enhanced endocytosis, AβOs impair NLGN1/2- and LRRTM2-mediated presynaptic organization.
