ArticleNeurology(R) neuroimmunology & neuroinflammation2026
IgM Anti-Ganglioside Binding and Complement Activation in an iPSC-Derived Motor Neuron Model for Multifocal Motor Neuropathy.
Article in Neurology(R) neuroimmunology & neuroinflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesMultifocal motor neuropathy (MMN) is an asymmetric motor neuropathy driven by IgM autoantibodies targeting gangliosides, particularly GM1. In this study, we investigated the relationship between IgM seropositivity, complement activation, and clinical parameters using an induced pluripotent stem cell (iPSC)-derived motor neuron (MN) model of MMN.
methodsWe used serum samples from 137 patients with MMN to assess IgM binding and subsequent C3 fixation to iPSC MNs and their correlation with clinical parameters, including muscle strength expressed as MRC sum scores, obtained from patient records. In addition, we tested the efficacy of IV immunoglobulin (IVIg) and specific complement inhibitors to prevent C3 fixation to MNs.
resultsWe observed increased IgM binding to iPSC MNs using serum samples from patients with MMN compared with those from healthy controls, which correlated with IgM anti-ganglioside antibody titers. Higher antibody binding correlated with levels of C3 fixation, more severe weakness, and the need for higher IVIg doses. Complement activation, but not IgM binding, also correlated with vibration sense abnormalities, brachial plexus MRI abnormalities, and the degree of axonal damage. At therapeutic concentrations, IVIg moderately inhibited complement activation (34%-54%) while specific complement inhibitors were highly effective (89.1%-98.7%) in the iPSC MN model. DISCUSSION: This study demonstrates that IgM antibodies in serum samples from patients with MMN induce complement activation on iPSC MNs, which correlates significantly with clinical outcomes. In addition, our findings indicate that complement inhibitors offer a potentially targeted novel therapeutic strategy for MMN and that our iPSC MN model is a viable preclinical screening platform.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.