Miguel Angel Baca
Research Subjects
Research Interests
Miguel Angel Baca has a total of 11 co-authors. Here are the top co-authors by number of shared publications:
- Ana Rivas
Department of Nutrition and Food Science, University of Granada, Granada, Spain; "José Mataix Verdú" Institute of Nutrition and Food Technology (INYTA), Biomedical Research Centre (CIBM), University of Granada, Granada, Spain; Instituto de Investigación Biosanitaria ibs.GRANADA, Granada, Spain
3 shared publications - Celia Monteagudo
Department of Nutrition and Food Science, University of Granada, Granada, Spain; "José Mataix Verdú" Institute of Nutrition and Food Technology (INYTA), Biomedical Research Centre (CIBM), University of Granada, Granada, Spain; Instituto de Investigación Biosanitaria ibs.GRANADA, Granada, Spain
3 shared publications - Pablo González-Domenech
Avenida de la Investigación nº 11, University of Granada, Granada, Spain
3 shared publications - Patricia González-Palacios
Department of Nutrition and Food Science, University of Granada, Granada, Spain; "José Mataix Verdú" Institute of Nutrition and Food Technology (INYTA), Biomedical Research Centre (CIBM), University of Granada, Granada, Spain
3 shared publications - Viviana Ramírez
Department of Nutrition and Food Science, University of Granada, Granada, Spain; "José Mataix Verdú" Institute of Nutrition and Food Technology (INYTA), Biomedical Research Centre (CIBM), University of Granada, Granada, Spain; Instituto de Investigación Biosanitaria ibs. GRANADA, Granada, Spain
3 shared publications - Alberto Zafra Gómez
José Mataix Verdú" Institute of Nutrition and Food Technology (INYTA), Biomedical Research Centre (CIBM), University of Granada, Granada, Spain; Instituto de Investigación Biosanitaria ibs.GRANADA, Granada, Spain; Department of Analytical Chemistry, University of Granada, Granada, Spain
1 shared publication
Latest Publications
- Open Access
- 8 October 2025
- Published by Elsevier in Journal of Affective Disorders
- Vol. 393 (Pt A) , 120410
Influence of childhood excess weight on cognitive, behavioural and emotional outcomes
- 8 October 2025
- Published by Elsevier in Journal of Affective Disorders
- Vol. 393 (Pt A) , 120410
Open AccessInfluence of childhood excess weight on cognitive, behavioural and emotional outcomes
- Open Access
- 17 September 2025
- Published by Elsevier in Science of The Total Environment
- Vol. 1001, 180434
The effect of paraben exposure on cognitive and behavioral outcomes in school children
- 17 September 2025
- Published by Elsevier in Science of The Total Environment
- Vol. 1001, 180434
Open AccessThe effect of paraben exposure on cognitive and behavioral outcomes in school children
- Open Access
Influence of Genetic Polymorphisms on Cognitive Function According to Dietary Exposure to Bisphenols in a Sample of Spanish Schoolchildren
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.
Open AccessInfluence of Genetic Polymorphisms on Cognitive Function According to Dietary Exposure to Bisphenols in a Sample of Spanish Schoolchildren
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.