The brain is a very complex organ. It is said to be the most complex part of the human body. It is also known as the seat of intelligence and it involves biological processes that control sight, hearing, speech, memory, cognition, sensation, movement, and a whole lot of other things. The brain is made up of billions of nerves and other structures that participate in holistic functioning. Receptors like the NMDAR are essential for learning and memory. Sometimes, conditions like autoimmune disorders can disrupt normal functioning in the brain. This is a situation where the body produces antibodies against its healthy cells, which can lead to cell destruction. N-methyl D-aspartate receptor (NMDAR) encephalitis is an autoimmune disorder caused by the attack of autoantibodies on the GluN1 subunit of the NMDA receptor leading to a decrease in NMDAR and various neuropsychiatric symptoms.
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Antibodies could result in deterioration.
This is the commonest antibody-mediated encephalitis. The acute stage involves neuropsychiatric symptoms like seizures, short-term memory loss, abnormal movements, and decreased level of consciousness. This is followed by a resolution of these symptoms which takes some months to years. A study was carried out by a group of scientists to connect the reduced amount of NMDA to progressive memory deficit. According to theory, patients’ NMDAR antibodies cause the network state to be permanently disrupted after only a brief period of hippocampus exposure.
Mice were used as test subjects and all patients gave their consent for their CSF to be used. NMDAR was injected. The data was analyzed using calcium imaging. The findings indicate that the presence of abnormal CA1 neuronal activity was noticed after NMDAR infusion. It was discovered that anti-NMDAR reduced the capacity for behaviorally recalling both old and new memories, with a major memory impairment occurring early on in the recovery period. A loss of spatial information brought on by the presence of antibodies was established. Results indicate that in the mouse test subjects, before and after the infusion of antibodies for old and newly acquired memories, the hippocampus spatial information is reduced in anti-NMDAR groups. Also, these results demonstrate that the presence of NMDAR antibodies causes the neuronal correlate of new memories to deteriorate over periods of 4 hours.
Clinical significance
With the knowledge of these findings, new treatment modalities for anti-NMDAR encephalitis can be formulated. The behavioral and long-memory alterations of the disease can be treated. Immunization against the GluN1 antibodies can be very useful and could be associated with neuroprotective effects.
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Conclusion
The future of N-methyl D-aspartate receptor (NMDAR) encephalitis management looks rosy. Findings prove that the antibodies against NMDAR cause long-term memory loss and unusual behavior. With the knowledge of these facts, new therapeutic approaches could emerge and alter the situation.
