ReviewMetabolic brain disease2026
The gut-brain axis in arsenic-induced toxicity: mechanisms, consequences, and therapeutic perspectives.
Review in Metabolic brain disease, 2026. 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.
- Mapping the multigenomic human system: structural asymmetry and interface gaps in host-exogenous biological interactions.Frontiers in microbiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic ingestion of arsenic frequently occurring in contaminated groundwater poses a serious dual threat to neurological health. Environmental toxicants present in groundwater are highly correlated with onset of neuropathological effects through complex gut-brain axis interactions. The systematic review of literature aims evaluate the neurobehavioural consequences and molecular outcome of a groundwater contaminant, arsenic with microbiota alteration involving animal studies and epidemiological data. Arsenic disrupts the gut microbiota, diminishing beneficial bacteria and promoting harmful strains, which in turn compromise gut barrier integrity, trigger inflammation and oxidative stress, leading to alteration in critical metabolic pathways involved in neurotransmitter production and mitochondrial function. Animal studies have shown that chronic exposure intensifies these effects, causing more pronounced microbial dysbiosis alongside worsened cognitive and behavioural deficits. Mechanistically, arsenic impairs neural signaling by elevating reactive oxygen species, disrupting synaptic and mitochondrial dynamics, and inducing neuroinflammation after its accumulation in brain tissues, while gut-derived neuroactive compounds exacerbate neuroinflammation and neuronal damage irrespective of significant arsenic deposition in the brain. Therapeutic strategies that reinforce gut health, such as targeted probiotic and prebiotic supplementation have demonstrated the ability to restore microbiome balance, strengthen barrier function, reduce neuroinflammatory markers and improve behavioural outcomes in experimental models. These microbiota-focused interventions, when combined with conventional measures like chelation to remove toxic metals and the deployment of water treatment infrastructure in affected regions, suggest a powerful integrated approach. By addressing both the source of contamination and the downstream biological consequences, this multimodal strategy holds significant promise for mitigating arsenic-induced neurotoxicity and protecting at-risk populations in affected communities.
Indexed as
Identifiers
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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.