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(A) Synaptic NMDARs interact with EphB2; patients’ antibodies bind to NMDARs. (B) After patients’ antibody binding, the NMDAR – EphB2 interaction is disrupted. NMDARs leave synapses, are cross-linked, and internalized. (C) Patients’ antibodies reduce synaptic NMDAR currents and impair LTP induction. These electrophysiologic effects are linked to the clinical symptoms of the disease, including amnesia, psychosis, seizures, and dyskinetic movements.
