ArticleiScience2023
Prenatal low-dose methylmercury exposure causes premature neuronal differentiation and autism-like behaviors in a rodent model.
Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Benzo[a]pyrene-induced AHR activation in human ESCs primes premature neurogenesis in cerebral organoids.Journal of hazardous materials · 2026Article
- Mercury-induced excitotoxicity in autism spectrum disorder: disruption of glutamatergic homeostasis and the therapeutic role of the selenium-glutathione axis.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- Impact of prenatal environmental exposure on offspring neurodevelopment and susceptibility to neurodegenerative diseases: mechanisms and perspectives.Frontiers in public health · 2026Review
- Methylmercury exposure at dosage conditions that do not affect growth can impair memory in adolescent mice.Toxicological research · 2024Article
- Reduction of Glyoxalase 1 Expression Links Fetal Methylmercury Exposure to Autism Spectrum Disorder Pathogenesis.Toxics · 2024Article
- Single-cell investigation of lead toxicity from neurodevelopment to neurodegeneration: Current review and future opportunities.Current opinion in toxicology · 2024Article
- A bibliometric analysis of autism spectrum disorder signaling pathways research in the past decade.Frontiers in psychiatry · 2024Article
- Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant neurodevelopment is a core deficit of autism spectrum disorder (ASD). Here we ask whether a non-genetic factor, prenatal exposure to the environmental pollutant methylmercury (MeHg), is a contributing factor in ASD onset. We showed that adult mice prenatally exposed to non-apoptotic MeHg exhibited key ASD characteristics, including impaired communication, reduced sociability, and increased restrictive repetitive behaviors, whereas in the embryonic cortex, prenatal MeHg exposure caused premature neuronal differentiation. Further single-cell RNA sequencing (scRNA-seq) analysis disclosed that prenatal exposure to MeHg resulted in cortical radial glial precursors (RGPs) favoring asymmetric differentiation to directly generate cortical neurons, omitting the intermediate progenitor stage. In addition, MeHg exposure in cultured RGPs increased CREB phosphorylation and enhanced the interaction between CREB and CREB binding protein (CBP). Intriguingly, metformin, an FDA-approved drug, can reverse MeHg-induced premature neuronal differentiation via CREB/CBP repulsion. These findings provide insights into ASD etiology, its underlying mechanism, and a potential therapeutic strategy.
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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.