# Influence of Genetic Polymorphisms on Cognitive Function According to Dietary Exposure to Bisphenols in a Sample of Spanish Schoolchildren

**Authors:** Viviana Ramírez, Patricia González-Palacios, Pablo José González-Domenech, Sonia Jaimez-Pérez, Miguel A. Baca, Lourdes Rodrigo, María Jesús Álvarez-Cubero, Celia Monteagudo, Luis Javier Martínez-González, Ana Rivas

PMC · DOI: 10.3390/nu16162639 · Nutrients · 2024-08-10

## TL;DR

This study shows how genetic differences and exposure to bisphenols in diet can affect cognitive abilities in Spanish schoolchildren.

## Contribution

The study is the first to show how genetic variability and bisphenol exposure interact to influence cognitive function in children.

## Key findings

- Certain BDNF and SNAP25 gene variants were linked to better fluid reasoning scores in children.
- Several SNPs interacted with bisphenol exposure to affect verbal comprehension, working memory, and fluid reasoning.
- The study highlights the importance of gene-environment interactions in neurodevelopmental outcomes.

## Abstract

Background: Neurodevelopmental disorders (NDDs) like intellectual disability (ID) are highly heritable, but the environment plays an important role. For example, endocrine disrupting chemicals (EDCs), including bisphenol A (BPA) and its analogues, have been termed neuroendocrine disruptors. This study aimed to evaluate the influence of different genetic polymorphisms (SNPs) on cognitive function in Spanish schoolchildren according to dietary bisphenol exposure. Methods: A total of 102 children aged 6–12 years old were included. Ten SNPs in genes involved in brain development, synaptic plasticity, and neurotransmission (BDNF, NTRK2, HTR2A, MTHFR, OXTR, SLC6A2, and SNAP25) were genotyped. Then, dietary exposure to bisphenols (BPA plus BPS) was estimated and cognitive functions were assessed using the WISC-V Spanish form. Results: BDNF rs11030101-T and SNAP25 rs363039-A allele carriers scored better on the fluid reasoning domain, except for those inheriting the BDNF rs6265-A allele, who had lower scores. Secondly, relevant SNP–bisphenol interactions existed in verbal comprehension (NTRK2 rs10868235 (p-int = 0.043)), working memory (HTR2A rs7997012 (p-int = 0.002), MTHFR rs1801133 (p-int = 0.026), and OXTR rs53576 (p-int = 0.030)) and fluid reasoning (SLC6A2 rs998424 (p-int = 0.004)). Conclusions: Our findings provide the first proof that exploring the synergistic or additive effects between genetic variability and bisphenol exposure on cognitive function could lead to a better understanding of the multifactorial and polygenic aetiology of NDDs.

## Linked entities

- **Genes:** BDNF (brain derived neurotrophic factor) [NCBI Gene 627], NTRK2 (neurotrophic receptor tyrosine kinase 2) [NCBI Gene 4915], HTR2A (5-hydroxytryptamine receptor 2A) [NCBI Gene 3356], MTHFR (methylenetetrahydrofolate reductase) [NCBI Gene 4524], OXTR (oxytocin receptor) [NCBI Gene 5021], SLC6A2 (solute carrier family 6 member 2) [NCBI Gene 6530], SNAP25 (synaptosome associated protein 25) [NCBI Gene 6616]
- **Chemicals:** bisphenol A (PubChem CID 6623), BPA (PubChem CID 6623)
- **Diseases:** intellectual disability (MONDO:0001071)

## Full-text entities

- **Genes:** OXTR (oxytocin receptor) [NCBI Gene 5021] {aka OT-R, OTR}, MTHFR (methylenetetrahydrofolate reductase) [NCBI Gene 4524], HTR2A (5-hydroxytryptamine receptor 2A) [NCBI Gene 3356] {aka 5-HT2A, HTR2}, NTRK2 (neurotrophic receptor tyrosine kinase 2) [NCBI Gene 4915] {aka DEE58, EIEE58, GP145-TrkB, OBHD, TRKB, trk-B}, SNAP25 (synaptosome associated protein 25) [NCBI Gene 6616] {aka CMS18, DEE117, RIC-4, RIC4, SEC9, SNAP}, BDNF (brain derived neurotrophic factor) [NCBI Gene 627] {aka ANON2, BULN2}, SLC6A2 (solute carrier family 6 member 2) [NCBI Gene 6530] {aka NAT1, NET, NET1, SLC6A5}
- **Diseases:** ID (MESH:D008607), NDDs (MESH:D002658), neuroendocrine disruptors (MESH:D018358)
- **Mutations:** rs11030101, rs6265, rs53576, rs1801133, rs7997012, rs363039, rs998424, rs10868235

## Full text

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## Figures

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## References

56 references — full list in the complete paper: https://tomesphere.com/paper/PMC11357571/full.md

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Source: https://tomesphere.com/paper/PMC11357571