SynthesisInternational journal of molecular sciences2026
The Possible Association Between Bisphenol A (BPA) and the Neuropathological Processes Characteristic of Alzheimer's Disease-A Systematic Review of the Literature.
Synthesis in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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2 authors.
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Abstract
Bisphenol A (BPA) is a ubiquitous environmental endocrine-disrupting compound whose potential neurotoxicity is attracting increasing interest. A growing body of evidence suggests a possible link between BPA exposure and neurodegenerative processes; however, comprehensive analyses of its role in Alzheimer's disease (AD) are lacking. The aim of this systematic review was to evaluate the available scientific evidence regarding the association between BPA exposure and Alzheimer's disease. A systematic literature review was conducted in accordance with the PRISMA 2020 guidelines. The PubMed/MEDLINE, Scopus, and Web of Science databases were searched up to 23 July 2026. Original research articles and meta-analyses published in English were included, covering studies in humans and animal models that analyzed the effects of BPA on Alzheimer's disease or related mechanisms. Study selection and data extraction were performed independently by two reviewers. The risk of bias was assessed using the ROBINS-E and SYRCLE tools. Of the 70 publications identified, 12 studies were included in the analysis. Most data came from in vivo and in vitro studies, and one study was clinical in nature (autopsy-based). The findings indicate that BPA exposure is associated with cognitive dysfunction, increased oxidative stress and neuroinflammation, amyloid-β accumulation, and tau protein hyperphosphorylation. Identified mechanisms included, among others, disturbances in insulin signaling, activation of the NF-κB and STAT3 pathways, and mitochondrial dysfunction. Eighty percent of the studies were rated as having good methodological quality. The analysis was limited by study heterogeneity, the small number of clinical studies, and the inability to perform a meta-analysis. The predominance of animal models and the use of high BPA doses hinder the direct extrapolation of the results to the human population. The available evidence suggests a possible association between BPA exposure and neuropathological processes characteristic of Alzheimer's disease. However, further well-designed epidemiological studies are needed to assess the impact of long-term, low-dose BPA exposure on the risk of developing AD.
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