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Autoimmune encephalitis (AE) is a rapidly expanding category of immune-mediated brain inflammation driven by autoantibodies targeting neuronal surface antigens or synaptic proteins: anti-NMDAR (most common — GluN1 subunit, often paraneoplastic ovarian teratoma in young women), anti-LGI1 (limbic encephalitis, VGKC complex, faciobrachial dystonic seizures), anti-CASPR2, anti-AMPAR, anti-GABA-B, anti-GABA-A, anti-NMDAR2; mechanisms: complement C1q/C3/C5b-9 membrane attack complex neuronal injury, NF-kB/IL-6/IL-17/IFN-gamma glial activation, microglial/astrocyte NLRP3 inflammasome, BBB disruption via MMP-9/TGF-beta1, CD8+ T cell neuronal cytotoxicity, receptor endocytosis/internalization, altered LTP/LTD (NMDAR endocytosis → psychosis/catatonia); clinical: psychiatric prodrome (psychosis, behavioral change), anterograde amnesia (limbic), movement disorders (orofacial dyskinesias, chorea, catatonia), autonomic dysfunction (tachy/bradycardia, hyperthermia), seizures, decreased consciousness; CASPR2 → Morvan syndrome (insomnia + peripheral nerve); CSF/MRI/EEG workup; tumor search mandatory. Sea moss fucoidan modulates NF-kB, BBB MMP-9/TGF-beta1, IL-6/IL-17, complement C1q/C3, NLRP3 microglial; selenium supports neural GPx1/GPx4 antioxidant defense; omega-3 DHA supports neuronal membrane phospholipid neuroprotection; zinc supports NMDAR co-agonist glycine/zinc modulation and BBB metalloenzymes. IVIG + plasmapheresis + high-dose methylprednisolone first-line; rituximab second-line; cyclophosphamide refractory; tumor resection if paraneoplastic (dramatic improvement); bortezomib/daratumumab plasma cell-depleting emerging.
