ReviewBiological trace element research2026
Neuro-inflammation Induced by Arsenic: An Insight into Mechanisms and Pathways Involved.
Review in Biological trace element research, 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.
- Environmental determinants of neurotoxicity: role of heavy metals in neurological disorders.Frontiers in neurology · 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroinflammation is increasingly recognized as a critical factor in the progression of various neurological disorders, with chronic exposure to environmental toxicants like arsenic emerging as a major contributor. This review focuses on arsenic-induced neuroinflammation, highlighting its underlying molecular mechanisms and pathways, global epidemiological burden, and current strategies for effective management. Arsenic groundwater contamination, particularly prevalent in Asian countries, poses a significant health risk to millions across more than 100 nations. Chronic exposure to arsenic generates reactive oxygen species (ROS), triggering oxidative stress and activating microglia, the key drivers of neuroinflammation. This cascade promotes proinflammatory cytokine release, leading to cognitive and neurological impairments. This review examines the underlying mechanisms, including mitochondrial dysfunction, oxidative damage, and inflammatory signaling pathways. Additionally, this review highlights current therapeutic strategies aimed at mitigating arsenic-induced neurotoxicity, including chelation therapy, natural antioxidants, and supplementation with essential trace elements. By addressing the multifactorial mechanisms underlying arsenic-induced neuroinflammation, the review emphasizes the urgent need for integrated public health initiatives and targeted interventions to alleviate the neurological consequences of chronic arsenic exposure.
Indexed as
Identifiers
40587075What 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.