Neurofascin (NF) is an L1 family immunoglobulin cell adhesion molecule (L1CAM) that exists in several different isoforms: nodal/neuronal NF140 (embyronal isoform) and NF186 and paranodal/glial NF155.  NF autoantibodies are associated with central and peripheral demyelinating disorders.  Passive transfer experiments in animal models have demonstrated that while not pathogenic if transferred alone, NF autoantibodies when cotransferred in animals induced with experimental autoimmune encephalitis (EAE) or experimental allergic neuritis (EAN): exacerbate disease severity and duration (EAE and EAN), exacerbate axonal injury (EAE), and cause conduction deficits (EAN).

Seropositivity to NF has been demonstrated in a minority of patients with MS, GBS, and CIDP.  Perhaps the best characterized disorder is CIDP associated with IgG4 anti-NF155, which is characterized by young age, subacute and severe onset, disabling tremor, distal weakness, poor response to IVIg, and encouraging response to rituximab.  Nodopathy associated with IgG anti-NF140/186 (targeting the common immunoglobulin domain amongst isoforms) has also been described.  More recently, NF autoantibody seropositivity has even been reported in hereditary and idiopathic neuropathy.