miR-26b, miR-30e, and miR-206 polymorphisms may play a role in BDNF-mediated development of Alzheimer-type dementia |
Ayten Tuna 1,1,1, Olcay Boyacioglu 2,2,2, Ayse Dondu 3,3,3, Seda Orenay-Boyacioglu 4,4,4,* |
1Aydin Adnan Menderes University Institute of Health Sciences Molecular Biotechnology Program, 2Aydin Adnan Menderes University Faculty of Engineering, 3Aydin Adnan Menderes University Faculty of Medicine Department of Psychiatry, 4Aydin Adnan Menderes University Faculty of Medicine Department of Medical Genetics |
Abstract
Objective:The Brain-Derived Neurotrophic Factor (BDNF) playing a crucial role in neuron survival and function, particularly in neurodegenerative diseases like Alzheimer's (AD). Our study seeks to explore polymorphisms in miRNAs that regulate the BDNF gene in individuals with AD, and to reveal the relationship between these polymorphisms and APOE genotypes.
Methods:Seventy AD patients who applied to the Psychiatry outpatient clinic were recruited for the study as well as 70 healthy individuals in the same age. The cases were examined for 5 miRNAs regulating BDNF and 2 APOE SNPs using the SNPType method on the Fluidigm platform.
Results:In comparisons of the genotype distributions for three polymorphisms (miR-206, miR-30e, miR-26b) and the allele frequencies for two polymorphisms (miR-30e, miR-206) detected significant differences between groups. While the APOE ε4/ε4 genotype was detected in 5% of the AD group, no individual with this genotype was observed in the control group. When the correlation between miRNA polymorphisms and APOE genotypic distributions were investigated, the miR-30e rs10489167 polymorphism showed a statistically significant positive correlation with the ε3/ε3 genotype and a statistically significant negative correlation with the ε2/ε3 genotype. On the other hand, the miR-30e rs112439044 polymorphism exhibited a statistically significant positive correlation with the ε2/ε2 and ε3/ε3 genotypes. In genetic inheritance models, miR-30e rs112439044 showed:1.52-fold risk in dominant, 22.92-fold in recessive, and 3.11-fold in additive models. miR-26b rs188612260 had a 2.04-fold risk in the additive model, while miR-206 rs16882131 showed 11.56-fold risk in the recessive model.
Conclusion:These findings could potentially offer insights into the mechanisms underlying AD.
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Accepted Manuscript [Submitted on 2024-07-09, Accepted on 2024-10-08] |
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