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Potential NDMAR Antibody-Associated Mechanism in Orofacial Tardive Dyskinesia
Antibodies against neuronal N-methyl-D-aspartate receptor (NMDAR) may be associated with orofacial tardive dyskinesia (TD) and could potentially be mediated by increased choroid plexus (CP) volume. Researchers recently published their in the Journal of Psychiatric Research.
“Immune disturbance has been postulated to be one of the mechanisms underlying the pathogenesis of TD. Recently, the role of autoimmune abnormality in TD has been increasingly recognized,” Na Li, Peking University HuiLongGuan Clinical Medical School, Beijing HuiLongGuan Hospital, China, et al wrote. “Autoantibodies against neuronal NMDAR may be cross-reactive in the brain in neuropsychiatric disorders, and the CP is a crucial immune barrier in the central nervous system (CNS).”
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Researchers assessed the serum NMDAR antibody levels by enzyme-linked immunosorbent assay. In schizophrenia patients with TD, they assessed CP and ventricle volumes by magnetic resonance imaging. Study participants consisted of 122 patients with schizophrenia, 61 with TD, 61 without TD (NTD), compared with 74 healthy controls. Using the Positive and Negative Syndrome Scale and Abnormal Involuntary Movement Scale (AIMS), psychopathology and TD severity were evaluated
Compared with the NTD group, the TD group had significantly higher NMDAR antibody levels and CP volumes. Higher NMDAR antibody level was correlated with larger CP volume in the TD group. An elevated NMDAR antibody level and enlarged CP volume were correlated with orofacial AIMS score and in a mediation model, the CP volume mediated the effect of NMDAR antibody level on the orofacial AIMS score.
“Our findings highlight a potential NMDAR antibody-associated mechanism in orofacial TD, which may be mediated by increased CP volume,” Na Li et al concluded.
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