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Anti-NMDAR Antibodies: Autoimmune Mediators of Encephalitis

Molecular Structure and Target Recognition

Anti-NMDAR (N-methyl-D-aspartate receptor) antibodies are autoantibodies that target specific components of the NMDA receptor, particularly:

  • GluN1 subunit (primary target)
  • Conformational epitopes
  • Extracellular domains

These antibodies are predominantly IgG class, with IgG1 and IgG3 subclasses being the most common. Their binding leads to:

  • Receptor crosslinking
  • Internalization of NMDA receptors
  • Reduction in synaptic NMDAR density

Pathophysiological Mechanisms

Receptor Interaction

The antibodies affect NMDA receptor function through multiple mechanisms:

Direct Effects: Receptor internalization, Decreased receptor density, Altered synaptic plasticity

Synaptic Changes: Reduced glutamatergic transmission, Disrupted synaptic function, Impaired long-term potentiation

Neurological Impact

The presence of these antibodies leads to:

  • Disrupted neurotransmitter signalling
  • Altered neural network function
  • Compromised synaptic plasticity
  • Neuroinflammatory responses

Clinical Manifestations

Anti-NMDAR Encephalitis

Early Symptoms: Psychiatric manifestations, Behavioural changes, Memory deficits, Anxiety and agitation

Progressive Symptoms: Seizures, Movement disorders, Autonomic instability, Decreased consciousness

Associated Conditions

The antibodies are often associated with:

  • Ovarian teratomas
  • Other autoimmune disorders
  • Viral infections
  • Paraneoplastic syndromes

Diagnostic Approaches

Laboratory Testing

CSF Analysis: Antibody detection, Inflammatory markers, Cell count and protein levels

Serum Testing: Antibody titters, Immunological markers, Inflammatory indicators

Imaging Studies

  1. MRI brain imaging
  2. PET scanning
  3. EEG monitoring

Treatment Strategies and Prognosis

First-Line Treatments

Immunotherapy: Corticosteroids, Intravenous immunoglobulins, Plasma exchange

Tumor Removal: When applicable (especially teratomas), Surgical intervention, post-operative monitoring

Second-Line Treatments

For refractory cases:

  • Rituximab
  • Cyclophosphamide
  • Other immunosuppressants

Monitoring and Follow-up

Regular assessment of:

  • Clinical improvement
  • Antibody levels
  • Cognitive function
  • Neurological status

Research continues to expand our knowledge of:

  • Pathogenic mechanisms
  • Novel treatment approaches
  • Long-term outcomes
  • Prevention strategies

The prognosis varies but is generally favourable with early intervention. Recovery can be prolonged, requiring months to years of treatment and rehabilitation.

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