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Genetic polymorphism in BIN1 rather than APOE is associated with poor recognition memory among men without dementia

Although several genetic polymorphisms have been linked with the risk of Alzheimer’s disease, less is known about their impact on cognitive performance among cognitively healthy individuals. Our aim was to investigate the association of the genetic variant, rs744373 in the bridging integrator 1 gene...

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Autores principales: Mehta, Kanika, Mohebbi, Mohammadreza, Pasco, Julie A., Williams, Lana J., Walder, Ken, Ng, Boon Lung, Gupta, Veer Bala
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9592585/
https://www.ncbi.nlm.nih.gov/pubmed/36280690
http://dx.doi.org/10.1038/s41598-022-20587-9
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author Mehta, Kanika
Mohebbi, Mohammadreza
Pasco, Julie A.
Williams, Lana J.
Walder, Ken
Ng, Boon Lung
Gupta, Veer Bala
author_facet Mehta, Kanika
Mohebbi, Mohammadreza
Pasco, Julie A.
Williams, Lana J.
Walder, Ken
Ng, Boon Lung
Gupta, Veer Bala
author_sort Mehta, Kanika
collection PubMed
description Although several genetic polymorphisms have been linked with the risk of Alzheimer’s disease, less is known about their impact on cognitive performance among cognitively healthy individuals. Our aim was to investigate the association of the genetic variant, rs744373 in the bridging integrator 1 gene (BIN1), the strongest genetic risk factor for Alzheimer’s disease after the APOE ε4 allele, with different cognitive domains among non-demented older men. Cognitive function was measured using the CogState Brief Battery, which assessed cognitive performance across four domains: psychomotor function, visual attention, recognition memory and working memory. Linear regression analysis revealed that individuals with the BIN1 risk allele performed poorly on the recognition memory task as compared to those without the risk allele. However, this was in contrast with the individuals who harboured the APOE ε4 risk allele as they displayed better performance on the recognition task in comparison to those without the ε4 risk allele. To the best of our knowledge, this is the first study that demonstrates genetic variation in BIN1 to be a better predictor of recognition memory than APOE, which remains the biggest genetic risk factor for Alzheimer’s disease.
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spelling pubmed-95925852022-10-26 Genetic polymorphism in BIN1 rather than APOE is associated with poor recognition memory among men without dementia Mehta, Kanika Mohebbi, Mohammadreza Pasco, Julie A. Williams, Lana J. Walder, Ken Ng, Boon Lung Gupta, Veer Bala Sci Rep Article Although several genetic polymorphisms have been linked with the risk of Alzheimer’s disease, less is known about their impact on cognitive performance among cognitively healthy individuals. Our aim was to investigate the association of the genetic variant, rs744373 in the bridging integrator 1 gene (BIN1), the strongest genetic risk factor for Alzheimer’s disease after the APOE ε4 allele, with different cognitive domains among non-demented older men. Cognitive function was measured using the CogState Brief Battery, which assessed cognitive performance across four domains: psychomotor function, visual attention, recognition memory and working memory. Linear regression analysis revealed that individuals with the BIN1 risk allele performed poorly on the recognition memory task as compared to those without the risk allele. However, this was in contrast with the individuals who harboured the APOE ε4 risk allele as they displayed better performance on the recognition task in comparison to those without the ε4 risk allele. To the best of our knowledge, this is the first study that demonstrates genetic variation in BIN1 to be a better predictor of recognition memory than APOE, which remains the biggest genetic risk factor for Alzheimer’s disease. Nature Publishing Group UK 2022-10-24 /pmc/articles/PMC9592585/ /pubmed/36280690 http://dx.doi.org/10.1038/s41598-022-20587-9 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Mehta, Kanika
Mohebbi, Mohammadreza
Pasco, Julie A.
Williams, Lana J.
Walder, Ken
Ng, Boon Lung
Gupta, Veer Bala
Genetic polymorphism in BIN1 rather than APOE is associated with poor recognition memory among men without dementia
title Genetic polymorphism in BIN1 rather than APOE is associated with poor recognition memory among men without dementia
title_full Genetic polymorphism in BIN1 rather than APOE is associated with poor recognition memory among men without dementia
title_fullStr Genetic polymorphism in BIN1 rather than APOE is associated with poor recognition memory among men without dementia
title_full_unstemmed Genetic polymorphism in BIN1 rather than APOE is associated with poor recognition memory among men without dementia
title_short Genetic polymorphism in BIN1 rather than APOE is associated with poor recognition memory among men without dementia
title_sort genetic polymorphism in bin1 rather than apoe is associated with poor recognition memory among men without dementia
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9592585/
https://www.ncbi.nlm.nih.gov/pubmed/36280690
http://dx.doi.org/10.1038/s41598-022-20587-9
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