Neurotoxic Effects of Bisphenol (BPA): Mini-Reviews.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing preclinical animal and in vitro mechanistic studies
PubMed 41150587 · doi:10.3390/toxics13100888
What was done
Searches were conducted across PubMed, the Virtual Health Library (VHL/BVS), and ScienceDirect for articles published between 2007 and 2025 in English, Portuguese, or Spanish regarding Bisphenol A (BPA) neurotoxicity. Following screening, 12 articles evaluating animal models and cell cultures were included in this mini-review.
What was found
The abstract reports no quantitative summary metrics or specific effect sizes. Qualitatively, the 12 reviewed preclinical studies showed that BPA exposure reduced neuronal survival, dendritic density, and synaptic plasticity. In animal models, exposure was associated with memory and learning deficits, increased oxidative stress, and alterations in AMPK, HO-1, and nNOS/Keap1/Nrf2 pathways. In cell cultures, BPA induced apoptosis, autophagy dysfunction, cytoskeletal changes, and loss of synaptic proteins, showing dose-dependent and sex-dependent effects.
Why it matters
This review outlines the molecular and cellular mechanisms through which BPA may cause central nervous system toxicity. It adds synthesized preclinical rationale for re-evaluating regulatory exposure limits for plastic additives.
Limits
The review included only 12 studies and provided no meta-analytic pooling, formal quality appraisal, or quantitative effect sizes. Evidence is entirely derived from in vitro and animal models, precluding direct conclusions about human clinical outcomes or real-world exposure risks.
Cited by
- supports BPA induces oxidative stress and generates free radicals in the brain that impair synaptic plasticity.