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Memory in autoimmune NMDA receptor encephalitis: an issue for B cells and patients.

This scientific commentary refers to ‘Human cerebrospinal fluid monoclonal N -methyl-D-aspartate receptor autoantibodies are sufficient for encephalitis pathogenesis’, by Kreye et al. (doi:10.1093/brain/aww208) .

Autoimmune NMDA receptor (NMDAR) encephalitis was first described in 2007 as an immunotherapy-responsive syndrome that is often paraneoplastic. Ovarian teratoma is the most commonly associated tumour (Titulaer et al. , 2013). NMDAR encephalitis now serves as a pathophysiological and therapeutic paradigm for several newly recognized autoimmune synaptic disorders affecting the CNS. Its distinctive clinical spectrum includes psychiatric and behavioural manifestations, cognitive deficits, abnormal movements (particularly in children), seizures (most commonly as the initial manifestation in males), autonomic instability, central hypoventilation and altered consciousness (Titulaer et al. , 2013). IgG autoantibodies targeting the NR1 subunit of the NMDA receptor are implicated in the syndrome pathogenesis, and their detection—particularly in the CSF—aids diagnosis. The clinical benefit of therapies that reduce circulating antibody levels and B cell numbers supports the pathogenicity of NMDAR-IgG, as do experimental studies in vitro and in vivo . The binding of patients’ CSF IgG to live hippocampal neurons decreases the density of NMDAR clusters by inducing endocytosis and lysosomal degradation of antibody-NMDAR complexes. After the autoantibody is removed, newly synthesized NMDARs repopulate the plasma membrane. Endocytosis is accompanied by a selective reduction in synaptic NMDAR-mediated currents (Hughes et al. , 2010; Moscato et al. , 2014). Mice injected intrathecally with patients’ CSF exhibit memory impairments and behavioural abnormalities, while human NMDAR-specific IgG progressively …