ArticleJournal of neurology2026
Genetic modification of obesity-associated disability progression in multiple sclerosis.
Article in Journal of neurology, 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
5 authors.
Funding
Abstract
backgroundObesity has been associated with adverse outcomes in multiple sclerosis (MS), but whether its influence on disability progression differs according to immunogenetic background remains unclear. We investigated whether associations between obesity at diagnosis and subsequent disability progression vary by HLA-A*02:01 status.
methodsUsing data from two Swedish population-based case-control studies, we included 2117 individuals with MS, disease duration ≤5 years at study inclusion, and available HLA genotyping. Obesity was defined as body mass index (BMI) >30 kg/m
resultsAmong individuals lacking HLA-A*02:01, obesity was associated with an increased risk of CDW (HR 1.49, 95% CI 1.12-1.82), EDSS 3 (HR 1.90, 95% CI 1.30-2.79), and EDSS 4 (HR 2.30, 95% CI 1.33-3.73). No corresponding associations were observed among HLA-A02:01-positive individuals. Analyses treating BMI as a continuous variable yielded similar findings. Additive interaction analyses further supported a joint effect of obesity and absence of HLA-A*02:01 on disability progression. Longitudinal models demonstrated the highest predicted EDSS trajectories among obese HLA-A*02:01-negative individuals.
conclusionsObesity at diagnosis was associated with worse disability outcomes primarily among individuals lacking HLA-A*02:01, suggesting that HLA class I-related immune pathways may modify the influence of excess adiposity on MS disease progression.
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.