Tier 3 — preclinical

Betaine alleviates fluoride-induced learning and memory impairment in offspring rats through DNA methylation of GNAS

Yin Chen, Wei Wu, Lianhong Li, Man Wang, Xiaogang Zhang, Ling Tang, Yi Luo, Min Liu, Jun Liu
Ecotoxicology and environmental safety 2026 323:120722

Bibliography

PubMed
PMID 42691841
Funding
Funding was not specified in the indexed record or accessible funding metadata.
Competing interests
Reported disclosure: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Study snapshot

DesignExperimental animal and/or laboratory research
ModelPregnant rats and offspring
SampleExperiment-specific biological replicates and model groups; see original methods
InterventionMaternal betaine during fluoride exposure
DurationPregnancy exposure and offspring testing
EndpointsOffspring learning; GNAS methylation

What the study showed, in plain terms

Published in 2026, this source examined preclinical aging, brain and metabolic mechanisms. Design: Experimental animal and/or laboratory research. Sample/model: Experiment-specific biological replicates and model groups; see original methods. The exposure or intervention was Maternal betaine during fluoride exposure. Follow-up or treatment period: Pregnancy exposure and offspring testing.

Selected learning, hippocampal and GNAS-methylation changes favored betaine in the fluoride-exposed rat model.

Experimental model evidence. The intervention, concentrations and outcomes do not establish an effective human supplement dose or a clinical treatment benefit.

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Key findings

  • Selected learning, hippocampal and GNAS-methylation changes favored betaine in the fluoride-exposed rat model.
  • The recorded outcome domains were Offspring learning; GNAS methylation.
  • The result applies to the tested exposure: Maternal betaine during fluoride exposure; Pregnancy exposure and offspring testing.

What this study can and cannot tell us

  • Experimental model evidence. The intervention, concentrations and outcomes do not establish an effective human supplement dose or a clinical treatment benefit.
  • Cell concentrations, species, disease models and experimental routes cannot be converted directly into an effective or safe oral human regimen.
  • Source basis: Indexed abstract and bibliographic data. Missing method details, funding information or participant denominators are not inferred.

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