Interaction Between Arteriosclerosis and -β on Cognitive Function

IF 3.4 3区 医学 Q2 NEUROSCIENCES Journal of Alzheimer's Disease Pub Date : 2024-01-05 DOI:10.3233/jad-230604
I. Frentz, Joyce van Arendonk, A. Leeuwis, Meike W. Vernooij, W. M. van der Flier, Daniel Bos, P. P. De Deyn, F. Wolters, M. Ikram
{"title":"Interaction Between Arteriosclerosis and -β on Cognitive Function","authors":"I. Frentz, Joyce van Arendonk, A. Leeuwis, Meike W. Vernooij, W. M. van der Flier, Daniel Bos, P. P. De Deyn, F. Wolters, M. Ikram","doi":"10.3233/jad-230604","DOIUrl":null,"url":null,"abstract":"Background: Dementia is a multifactorial disease, with Alzheimer’s disease (AD) and vascular pathology often co-occurring in many individuals with dementia. Yet, the interplay between AD and vascular pathology in cognitive decline is largely undetermined. Objective: The aim of the present study was to examine the joint effect of arteriosclerosis and AD pathology on cognition in the general population without dementia. Methods: We determined the interaction between blood-based AD biomarkers and CT-defined arteriosclerosis on cognition in 2,229 dementia-free participants of the population-based Rotterdam Study (mean age: 68.9 years, 52% women) cross-sectionally. Results: Amyloid-β (Aβ)42 and arterial calcification were associated with cognitive performance. After further adjustment for confounders in a model that combined all biomarkers, only arterial calcification remained independently associated with cognition. There was a significant interaction between arterial calcification and Aβ 42 and between arterial calcification and the ratio of Aβ 42/40. Yet, estimates attenuated, and interactions were no longer statistically significant after adjustment for cardio metabolic risk factors. Conclusions: Arteriosclerosis and AD display additive interaction-effects on cognition in the general population, that are due in part to cardio metabolic risk factors. These findings suggest that joint assessment of arteriosclerosis and AD pathology is important for understanding of disease etiology in individuals with cognitive impairment.","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":null,"pages":null},"PeriodicalIF":3.4000,"publicationDate":"2024-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Alzheimer's Disease","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3233/jad-230604","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0

Abstract

Background: Dementia is a multifactorial disease, with Alzheimer’s disease (AD) and vascular pathology often co-occurring in many individuals with dementia. Yet, the interplay between AD and vascular pathology in cognitive decline is largely undetermined. Objective: The aim of the present study was to examine the joint effect of arteriosclerosis and AD pathology on cognition in the general population without dementia. Methods: We determined the interaction between blood-based AD biomarkers and CT-defined arteriosclerosis on cognition in 2,229 dementia-free participants of the population-based Rotterdam Study (mean age: 68.9 years, 52% women) cross-sectionally. Results: Amyloid-β (Aβ)42 and arterial calcification were associated with cognitive performance. After further adjustment for confounders in a model that combined all biomarkers, only arterial calcification remained independently associated with cognition. There was a significant interaction between arterial calcification and Aβ 42 and between arterial calcification and the ratio of Aβ 42/40. Yet, estimates attenuated, and interactions were no longer statistically significant after adjustment for cardio metabolic risk factors. Conclusions: Arteriosclerosis and AD display additive interaction-effects on cognition in the general population, that are due in part to cardio metabolic risk factors. These findings suggest that joint assessment of arteriosclerosis and AD pathology is important for understanding of disease etiology in individuals with cognitive impairment.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
动脉硬化与-β对认知功能的相互作用
背景:痴呆症是一种多因素疾病,在许多痴呆症患者中,阿尔茨海默病(AD)和血管病变往往同时存在。然而,认知能力下降过程中阿尔茨海默病和血管病理学之间的相互作用在很大程度上尚未确定。研究目的本研究旨在探讨动脉硬化和 AD 病变对无痴呆症的普通人群认知能力的共同影响。研究方法我们通过横截面研究确定了基于血液的注意力缺失症生物标志物和 CT 定义的动脉硬化对基于人群的鹿特丹研究中 2,229 名无痴呆症参与者(平均年龄:68.9 岁,52% 为女性)认知能力的交互作用。结果显示淀粉样蛋白-β(Aβ)42和动脉钙化与认知能力有关。在结合所有生物标志物的模型中进一步调整混杂因素后,只有动脉钙化仍与认知能力独立相关。动脉钙化与 Aβ 42 之间以及动脉钙化与 Aβ 42/40 的比率之间存在明显的交互作用。然而,在对心血管代谢风险因素进行调整后,估计值减弱,相互作用不再具有统计学意义。结论在普通人群中,动脉硬化和注意力缺失症对认知能力的交互影响是相加的,部分原因在于心脏代谢风险因素。这些发现表明,联合评估动脉硬化和注意力缺失症的病理变化对于了解认知障碍患者的疾病病因非常重要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Journal of Alzheimer's Disease
Journal of Alzheimer's Disease 医学-神经科学
CiteScore
6.40
自引率
7.50%
发文量
1327
审稿时长
2 months
期刊介绍: The Journal of Alzheimer''s Disease (JAD) is an international multidisciplinary journal to facilitate progress in understanding the etiology, pathogenesis, epidemiology, genetics, behavior, treatment and psychology of Alzheimer''s disease. The journal publishes research reports, reviews, short communications, hypotheses, ethics reviews, book reviews, and letters-to-the-editor. The journal is dedicated to providing an open forum for original research that will expedite our fundamental understanding of Alzheimer''s disease.
期刊最新文献
Endocrine Dyscrasia in the Etiology and Therapy of Alzheimer's Disease. Small Molecule Decoy of Amyloid-β Aggregation Blocks Activation of Microglia-Like Cells. A Novel Score to Predict Individual Risk for Future Alzheimer's Disease: A Longitudinal Study of the ADNI Cohort. Association of Plastic Exposure with Cognitive Function Among Chinese Older Adults. Gout or Hyperuricemia and Dementia Risk: A Meta-Analysis of Observational Studies.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1