ReviewNeurotoxicology2012
Methylmercury: a potential environmental risk factor contributing to epileptogenesis.
Review in Neurotoxicology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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
9 citing papers in PubMed, 26 citations in OpenAlex.
- The role of air pollution in epilepsy: a better understanding is needed.Arquivos de neuro-psiquiatria · 2025Review
- Review: myogenic and muscle toxicity targets of environmental methylmercury exposure.Archives of toxicology · 2024Review
- Mercury and Mercury-Containing Preparations: History of Use, Clinical Applications, Pharmacology, Toxicology, and Pharmacokinetics in Traditional Chinese Medicine.Frontiers in pharmacology · 2022Review
- Whole blood trace element and toxic metal concentration in dogs with idiopathic epilepsy and healthy dogs: A case-control study.Frontiers in veterinary science · 2022Article
- Cellular and Molecular Mechanisms Mediating Methylmercury Neurotoxicity and Neuroinflammation.International journal of molecular sciences · 2021Review
- The protein transportation pathway from Golgi to vacuoles via endosomes plays a role in enhancement of methylmercury toxicity.Scientific reports · 2014Article
- Response inhibition is impaired by developmental methylmercury exposure: acquisition of low-rate lever-pressing.Behavioural brain research · 2013Article
- Astrocytes protect neurons against methylmercury via ATP/P2Y(1) receptor-mediated pathways in astrocytes.PloS one · 2013Article
- Mechanisms and Modifiers of Methylmercury-Induced Neurotoxicity.Toxicology research · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Epilepsy or seizure disorder is one of the most common neurological diseases in humans. Although genetic mutations in ion channels and receptors and some other risk factors such as brain injury are linked to epileptogenesis, the underlying cause for the majority of epilepsy cases remains unknown. Gene-environment interactions are thought to play a critical role in the etiology of epilepsy. Exposure to environmental chemicals is an important risk factor. Methylmercury (MeHg) is a prominent environmental neurotoxicant, which targets primarily the central nervous system (CNS). Patients or animals with acute or chronic MeHg poisoning often display epileptic seizures or show increased susceptibility to seizures, suggesting that MeHg exposure may be associated with epileptogenesis. This mini-review highlights the effects of MeHg exposure, especially developmental exposure, on the susceptibility of humans and animals to seizures, and discusses the potential role of low level MeHg exposure in epileptogenesis. This review also proposes that a preferential effect of MeHg on the inhibitory GABAergic system, leading to disinhibition of excitatory glutamatergic function, may be one of the potential mechanisms underlying MeHg-induced changes in seizure susceptibility.
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.