From plastics to pathology: The neurodegenerative impact of Bisphenol-A on Alzheimer's disease.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing preclinical mechanisms and epidemiological evidence without systematic review methodology.
PubMed 42349722 · doi:10.1016/j.arr.2026.103219
What was done
This narrative review synthesized evidence from in vitro models, animal studies, and epidemiological research examining the impact of Bisphenol-A (BPA) exposure on Alzheimer's disease (AD) pathogenesis. The authors examined molecular pathways involving endocrine signaling, oxidative stress, neuroinflammation, synaptic plasticity, amyloid-beta accumulation, tau pathology, and cognitive decline, alongside evaluating BPA alternatives and preventive strategies.
What was found
The abstract provides no numerical data, effect sizes, or quantitative risk estimates. It qualitatively summarizes that BPA exposure promotes neurotoxicity and AD-related neuropathology by inducing oxidative stress, neuroinflammation, endocrine disruption, synaptic dysfunction, and the accumulation of amyloid-beta and tau.
Why it matters
The review outlines how ubiquitous environmental plasticizers may act as modifiable risk factors for neurodegeneration, highlighting molecular mechanisms to guide regulatory policy and future translational research.
Limits
As a narrative review, it lacks a systematic search protocol, risk-of-bias assessment, and meta-analytic quantification. Much of the underlying mechanistic data relies on in vitro and animal models with uncertain direct applicability to human clinical outcomes, and no primary sample sizes are reported.
Cited by
- supports BPA induces oxidative stress and generates free radicals in the brain that impair synaptic plasticity.