Cortical thickness is differently associated with ALDH2 rs671 polymorphism according to level of amyloid deposition
Abstract Accumulating evidence indicates that amyloid-beta (Aβ) deposition and biogenic aldehyde accumulation contribute to the pathogenesis of neurodegenerative diseases. Human aldehyde dehydrogenase 2 (ALDH2) metabolizes biogenic aldehydes produced in the brain to prevent damage. However, r671G>...
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2021
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oai:doaj.org-article:9047179a77954e6c919236a7bc74aa4e2021-12-02T17:18:21ZCortical thickness is differently associated with ALDH2 rs671 polymorphism according to level of amyloid deposition10.1038/s41598-021-98834-82045-2322https://doaj.org/article/9047179a77954e6c919236a7bc74aa4e2021-09-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-98834-8https://doaj.org/toc/2045-2322Abstract Accumulating evidence indicates that amyloid-beta (Aβ) deposition and biogenic aldehyde accumulation contribute to the pathogenesis of neurodegenerative diseases. Human aldehyde dehydrogenase 2 (ALDH2) metabolizes biogenic aldehydes produced in the brain to prevent damage. However, r671G>A, a single nucleotide polymorphism of ALDH2, causes aldehyde accumulation and decreased ALDH2 activity. We aimed to investigate whether Aβ deposition and rs671 polymorphism have an interaction effect on cortical thickness (CTh). We grouped 179 participants in the Biobank Innovations for chronic Cerebrovascular disease With ALZheimer's disease Study as follows: amyloid (–) [A(–)] and amyloid (+) [A(+)] groups based on the Aβ deposition degree; A-carrier (AC) and GG (GG) groups based on the presence/absence of the rs671 A allele; and their combinations, i.e., A(–)AC, A(–)GG, A(+)AC, and A(+)GG groups. A multiple regression analysis identified nine regions of interest. Compared with the A(–)GG group, the A(–)AC group showed thinner CTh in all regions. There were no significant differences between the A(+)AC and A(+)GG groups. We observed an interaction effect of amyloid deposition and rs671 polymorphism on CTh. The CTh in the A(–) group appeared to be strongly influenced by rs671 polymorphism, which could have contributed to cortical thinning and biogenic aldehyde accumulation in the AC group. Additionally, CTh in the A(+) group appeared to be strongly influenced by amyloid deposition.Yong Hyuk ChoHeirim LeeNa-Rae KimJin Wook ChoiHyun Woong RohJae Ho HaChang Hyung HongSang Won SeoSeong Hye ChoiEun-Joo KimByeong C. KimSeong Yoon KimJaeyoun CheongBumhee ParkSang Joon SonNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-10 (2021) |
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Medicine R Science Q Yong Hyuk Cho Heirim Lee Na-Rae Kim Jin Wook Choi Hyun Woong Roh Jae Ho Ha Chang Hyung Hong Sang Won Seo Seong Hye Choi Eun-Joo Kim Byeong C. Kim Seong Yoon Kim Jaeyoun Cheong Bumhee Park Sang Joon Son Cortical thickness is differently associated with ALDH2 rs671 polymorphism according to level of amyloid deposition |
description |
Abstract Accumulating evidence indicates that amyloid-beta (Aβ) deposition and biogenic aldehyde accumulation contribute to the pathogenesis of neurodegenerative diseases. Human aldehyde dehydrogenase 2 (ALDH2) metabolizes biogenic aldehydes produced in the brain to prevent damage. However, r671G>A, a single nucleotide polymorphism of ALDH2, causes aldehyde accumulation and decreased ALDH2 activity. We aimed to investigate whether Aβ deposition and rs671 polymorphism have an interaction effect on cortical thickness (CTh). We grouped 179 participants in the Biobank Innovations for chronic Cerebrovascular disease With ALZheimer's disease Study as follows: amyloid (–) [A(–)] and amyloid (+) [A(+)] groups based on the Aβ deposition degree; A-carrier (AC) and GG (GG) groups based on the presence/absence of the rs671 A allele; and their combinations, i.e., A(–)AC, A(–)GG, A(+)AC, and A(+)GG groups. A multiple regression analysis identified nine regions of interest. Compared with the A(–)GG group, the A(–)AC group showed thinner CTh in all regions. There were no significant differences between the A(+)AC and A(+)GG groups. We observed an interaction effect of amyloid deposition and rs671 polymorphism on CTh. The CTh in the A(–) group appeared to be strongly influenced by rs671 polymorphism, which could have contributed to cortical thinning and biogenic aldehyde accumulation in the AC group. Additionally, CTh in the A(+) group appeared to be strongly influenced by amyloid deposition. |
format |
article |
author |
Yong Hyuk Cho Heirim Lee Na-Rae Kim Jin Wook Choi Hyun Woong Roh Jae Ho Ha Chang Hyung Hong Sang Won Seo Seong Hye Choi Eun-Joo Kim Byeong C. Kim Seong Yoon Kim Jaeyoun Cheong Bumhee Park Sang Joon Son |
author_facet |
Yong Hyuk Cho Heirim Lee Na-Rae Kim Jin Wook Choi Hyun Woong Roh Jae Ho Ha Chang Hyung Hong Sang Won Seo Seong Hye Choi Eun-Joo Kim Byeong C. Kim Seong Yoon Kim Jaeyoun Cheong Bumhee Park Sang Joon Son |
author_sort |
Yong Hyuk Cho |
title |
Cortical thickness is differently associated with ALDH2 rs671 polymorphism according to level of amyloid deposition |
title_short |
Cortical thickness is differently associated with ALDH2 rs671 polymorphism according to level of amyloid deposition |
title_full |
Cortical thickness is differently associated with ALDH2 rs671 polymorphism according to level of amyloid deposition |
title_fullStr |
Cortical thickness is differently associated with ALDH2 rs671 polymorphism according to level of amyloid deposition |
title_full_unstemmed |
Cortical thickness is differently associated with ALDH2 rs671 polymorphism according to level of amyloid deposition |
title_sort |
cortical thickness is differently associated with aldh2 rs671 polymorphism according to level of amyloid deposition |
publisher |
Nature Portfolio |
publishDate |
2021 |
url |
https://doaj.org/article/9047179a77954e6c919236a7bc74aa4e |
work_keys_str_mv |
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1718381098416734208 |