ArticleBMC neurology2025
Causal associations between gut microbiota, metabolites, and idiopathic normal pressure hydrocephalus: a two‑sample Mendelian randomization study.
Article in BMC neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundImplying connections with gut microbiome and serum metabolites, idiopathic normal pressure hydrocephalus (INPH) emerges as a prevalent neuropsychiatric condition in the elderly. Our objective was to systematically evaluate the potential causality between gut microbiome, derived metabolites, and INPH through the implementation of Mendelian randomization (MR) methodology.
methodsWe utilized summary data from extensive genome-wide association studies, encompassing 196 gut microbiomes from the MiBioGen consortium (n = 18,340), 486 serum metabolites from the KORA and TwinsUK studies (n = 7,824), and individuals with INPH (case = 767, control = 375,610), for MR causal estimates. The leading analysis utilized the inverse-variance weighted (IVW) method, supplemented by weighted mode, MR-Egger, weighted median and simple mode approaches. Sensitivity analyses included MR-Egger intercept, Cochran's Q test, leave-one-out analysis and MR-PRESSO.
resultsOur study primarily relied on the IVW method, confirming a causality between 9 genetically predicted abundance of gut microbiomes and INPH. We found an adverse correlation with genetically predicted abundance of order Clostridiales, genus Eubacteriumeligensgroup, genus Gordonibacter, genus Ruminococcus1 concerning INPH. Conversely, class Melainabacteria, genus Eubacteriumruminantiumgroup, genus Adlercreutzia, genus Dialister, genus RikenellaceaeRC9gutgroup potentially correlated with increased INPH risk. As for derived metabolites, IVW estimates indicated a causal connection between 25 genetically predicted serum metabolites and INPH. Sensitivity analysis underscored the robustness of our findings.
conclusionOur MR analysis provides evidence supporting the causality of certain gut microbial taxa and their derived metabolites on INPH. This underscores the potential for interventions targeting specific gut microbiota and derived metabolites in the treatment and prevention of INPH.
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.