THE ROAD LESS TRAVELLED: EXPLORING PATHWAYS AS THERAPEUTIC GATEWAYS IN GUILLAIN-BARRÉ SYNDROME

Guillain-Barr Syndrome (GBS) is a rapidly progressive, immune-mediated neuropathy that can lead to paralysis, respiratory failure, and an increase in the proportion of cases, ultimately leading to death.Standard interventions, such as intravenous immunoglobulin (IVIg) and plasma exchange (TPE), provide broad immunomodulatory effects and have been the mainstay of care for decades.However, at present these treatments do not address all of the pathogenic mechanisms which are known to contribute to GBS, and many patients are left with persistent deficits.Recent advances have identified several additional pathways of interest, including complement activation, neonatal Fc receptor (FcRn)-mediated antibody recycling, ferroptosis, ERK/MAPK signalling, toll-like receptor activation, leukocyte migration across the blood-nerve barrier, and neuroendocrine-immune interactions.Novel therapeutic candidates targeting these mechanismssuch as the C1q inhibitor ANX005, the FcRn antagonist efgartigimod, the IgG-cleaving enzyme imlifidase, and complement C5 inhibitors -have demonstrated encouraging results in early clinical studies.Pre-clinical evidence also suggests that ferroptosis inhibitors, metabolic modulators, and immune-regulating hormone pathway interventions could provide additional therapeutic benefit.This review consolidates emerging evidence on both established and experimental GBS treatments, and outlines promising avenues for mechanism-based, disease-modifying therapies.