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NMDAR-antibody encephalitis is an autoimmune brain condition caused by patient’s own antibodies that bind to NMDA (N-Methyl-D-Aspartate) receptors in the synapses between nerve cells.

Laboratory studies have shown that these antibodies can cause NMDA receptors to be removed from the cell surface into the cell, interfering with signals between them.

But a new study has now shown this directly in patients with this condition.

The research, led by UCL working with a team from Oxford, involved specialised PET-magnetic resonance scans on five people recovering from the condition and 29 healthy volunteers.

It found that in the early phase of recovery the receptors are not as available in affected patients, but came back to normal levels after full recovery in another patient.

The paper has been published in JAMA Neurology and authored by a team including researchers from Oxford University’s Nuffield Department of Clinical Neuroscience (Professor Sarosh Irani) and the Department of Psychiatry (Dr Adam Al-Diwani).

Dr Al-Diwani said:


“Understanding the effect on receptors helps inform our understanding of how the antibodies cause the condition, and may help improve treatments in the future.”

Symptoms of NMDAR-antibody encephalitis include changes in mental state that can be confused with a psychiatric illness, before patients develop seizures and a movement disorder.