Autoimmune Neurological Disorders and Treatments

This study shows PNMA2 forms virus-like capsids that trigger an autoimmune response, leading to paraneoplastic neurological syndrome.

This study develops NMDA-receptor-Fc-fusion constructs that neutralize anti-NMDA receptor antibodies and inhibit their effects on neurons.

This study shows that anti-NMDAR encephalitis antibodies cause long-term hippocampal neuronal activity changes that persist after antibody clearance, leading to memory dysfunction.

The paper uses patient-derived autoantibodies to study LGI1 localization and interactome in mouse brains, revealing its synaptic distribution and novel protein complexes.

This study investigates functional connectivity changes in murine models of NMDAR antibody-associated pathology using rs-fMRI, finding impaired connectivity in hippocampal regions similar to human patients.

This study shows that an epitope-specific LGI1-autoantibody modulates Kv1.1 channel function, increasing neuronal excitability and potentially contributing to epileptiform activity.

The paper demonstrates that patient-derived monoclonal GABAA receptor antibodies cause catatonia and seizures in rodents, providing a model for autoimmune encephalitis and supporting antibody depletion as a treatment.

This study shows that chronic low-titer blood circulating anti-NMDAR1 autoantibodies impair spatial working memory in mice, suggesting potential cognitive effects in humans.

This study shows that anti-IgLON5 antibodies cause functional and neurodegenerative changes in human neurons, leading to cell death, supporting their role in the disease.

This study develops an active immunization model in mice that mimics anti-NMDA receptor encephalitis, revealing neuroinflammation and immune cell involvement in disease pathogenesis.

This study shows NMDA-receptor antibodies alter cortical microcircuit dynamics and predispose to paroxysmal EEG abnormalities in a mouse model.