ArticleDisease models & mechanisms2022
Bisphenol-A impairs synaptic formation and function by RGS4-mediated regulation of BDNF signaling in the cerebral cortex.
Article in Disease models & mechanisms, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- GenX exposure induces neurodevelopmental impairment and synaptic toxicity in hESC-derived cerebral organoids.Materials today. Bio · 2026Article
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- Kelulut honey (Toxicology reports · 2026Review
- Polyhexamethylene guanidine phosphate exposure induces abnormal behaviors by disrupting synaptic formation and activity in the cerebral cortex.Journal of neuroinflammation · 2026Article
- Differential Neurodevelopmental Disruption by Bisphenol A (BPA) and Valproic Acid (VPA) in Human Forebrain Organoids.bioRxiv : the preprint server for biology · 2026Article
- Environmental endocrine disruptors at the synapse: mechanisms linking chemical exposure to cognitive and behavioral dysfunction.Frontiers in behavioral neuroscience · 2026Review
- Integrated Multiomics Elucidates Molecular Mechanisms of Bisphenol A in Exacerbating Crohn's Disease.Mediators of inflammation · 2026Article
- Novel in silico Evidence of Bisphenol A as a Neuroinflammatory Modulator through the cGAS-STING-NLRP3 Pathway.Neurotoxicity research · 2025Article
- Bisphenol A Treatment Impairs Synaptic Function in Human Cholinergic Neurons.Journal of biochemical and molecular toxicology · 2025Article
- Investigating the Neuroprotective, Hepatoprotective, and Antimicrobial Effects of Mushroom Extracts.International journal of molecular sciences · 2025Article
- Taurine protection attenuates bisphenol-A-induced behavioral, neurochemical, and histopathological alterations in male rats.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Developmental neurotoxicity of bisphenol F and bisphenol S in animal model systems: A literature review.Neurotoxicology · 2025Review
- Non-genotoxic carcinogens (TPA and mezerein) activate tumourous transformation through miR let-7-mediated Hmga2 expression in Bhas42 cells.Environmental epigenetics · 2025Article
- Influence of Genetic Polymorphisms on Cognitive Function According to Dietary Exposure to Bisphenols in a Sample of Spanish Schoolchildren.Nutrients · 2024Article
- Prenatal Di-methoxyethyl phthalate exposure impairs cortical neurogenesis and synaptic activity in the mice.Brain pathology (Zurich, Switzerland) · 2024Article
- Effect of bisphenol A on the neurological system: a review update.Archives of toxicology · 2024Review
- Investigation of autism-related transcription factors underlying sex differences in the effects of bisphenol A on transcriptome profiles and synaptogenesis in the offspring hippocampus.Biology of sex differences · 2023Article
- Network analyses of upper and lower airway transcriptomes identify shared mechanisms among children with recurrent wheezing and school-age asthma.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bisphenol-A (BPA) is a representative endocrine disruptor, widely used in a variety of products including plastics, medical equipment and receipts. Hence, most people are exposed to BPA via the skin, digestive system or inhalation in everyday life. Furthermore, BPA crosses the blood-brain barrier and is linked to multiple neurological dysfunctions found in neurodegenerative and neuropsychological disorders. However, the mechanisms underlying BPA-associated neurological dysfunctions remain poorly understood. Here, we report that BPA exposure alters synapse morphology and function in the cerebral cortex. Cortical pyramidal neurons treated with BPA showed reduced size and number of dendrites and spines. The density of excitatory synapses was also decreased by BPA treatment. More importantly, we found that BPA disrupted normal synaptic transmission and cognitive behavior. RGS4 and its downstream BDNF/NTRK2 pathway appeared to mediate the effect of BPA on synaptic and neurological function. Our findings provide molecular mechanistic insights into anatomical and physiological neurotoxic consequences related to a potent endocrine modifier.
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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.