Anti-NMDA receptor encephalitis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
Anti-NMDA receptor encephalitis is predominantly caused by autoantibodies directed against the GluN1 component of the receptor. | |||
In the acute phase of brain diseases, B cells, plasma cells, CD4 T cells, and, less frequently, CD8 T cells have been detected. | |||
Crossing the blood-brain barrier enables systemically produced antibodies to crosslink NMDA receptors. This leads to their internalization and a severe disruption of synaptic plasticity and NMDA receptor network function. | |||
==References== | ==References== | ||
Revision as of 16:18, 10 December 2022
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Anti-NMDA receptor encephalitis Microchapters |
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Differentiating Anti-NMDA receptor encephalitis from Other Diseases |
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Diagnosis |
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Treatment |
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Case Studies |
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Anti-NMDA receptor encephalitis pathophysiology On the Web |
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American Roentgen Ray Society Images of Anti-NMDA receptor encephalitis pathophysiology |
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Directions to Hospitals Treating Anti-NMDA receptor encephalitis |
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Risk calculators and risk factors for Anti-NMDA receptor encephalitis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Anti-NMDA receptor encephalitis is predominantly caused by autoantibodies directed against the GluN1 component of the receptor.
In the acute phase of brain diseases, B cells, plasma cells, CD4 T cells, and, less frequently, CD8 T cells have been detected.
Crossing the blood-brain barrier enables systemically produced antibodies to crosslink NMDA receptors. This leads to their internalization and a severe disruption of synaptic plasticity and NMDA receptor network function.