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There is a strong potential in the use of body fluid biomarkers for different clinical purposes in neurological diseases. Such biomarkers can aid in diagnosis, prognosis, patient stratification and treatment effect monitoring. This value of biomarkers is exemplified by current use in diagnosis and follow-up of patients. This does for example include the analysis of cerebrospinal fluid (CSF) in Alzheimer´s disease for tau protein and abeta-peptides, the search for aquaporin autoantibodies in neuromyelitis optica. Rapid technological developments offer opportunities to develop novel and specific body fluid biomarkers, even in blood. This is shown by the use of blood neurofilament light chain in a variety of neurological diseases.

The established treatment options for CIDP are quite limited, to short term suppressive Ig based therapies (IVIG, SCIG, PLEX) and corticosteroids with their problematic long term side effects. The reasons behind this include disease rarity, heterogeneity, and that it is rarely life-threatening, all of which have contributed to the lack of an evidence base for other longer term and potentially more effective immunotherapies. Nonetheless other treatments often have to be tried in individual CIDP patients, without the trial evidence base. A knowledge base exists in other neurological diseases, including MG, MS and the MOG antibody and NMO variants. This gives some insights into which treatments should be considered and for which subgroups of CIDP, for how long an N=1 treatment trial should continue, and the comparative risks arising.

Cellular and humoral immune elements are invoked in the pathogenesis of inflammatory neuropathies, such as GBS and CIDP, and current opinion favors the pathogenic role of IgG autoantibodies in these conditions. The talk will review data supporting the critical role of activating FcγRs in experimental models of antibody- and T-cell orchestrated experimental models of inflammatory neuropathies. Modulation of these receptors is a potential treatment approach and a number of FcγR targeting therapies are at various stages of clinical development for such a strategy. Neonatal Fc receptor (FcRn) functions to protect IgG from catabolism and antagonism of this receptor can shorten the half-life of IgGs and IgG autoantibodies. Experimental studies will be reviewed that demonstrate that the FcRn antagonism shortens the half-life of circulating pathogenic anti-neural autoantibodies, which can reduce Ab-mediated nerve injury. In this context, FcRn inhibitors are at advanced stages of clinical development for various indications including CIDP.