Associations of accelerated biological ageing with incident dementia, cognitive functions and brain structure: a prospective cohort study based on UK Biobank.
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引用次数: 0
Abstract
Background: Several small-sample studies have suggested that biological processes of ageing are implicated with dementia and cognitive function. We aimed to prospectively investigate the associations of biological age with incident dementia, cognitive functions and brain structure based on the UK Biobank.
Methods: A total of 287 846 participants without dementia at baseline (followed until November 2022) were analysed. We measured biological age from clinical traits using the Klemera-Doubal method Biological Age (KDM-BA) and PhenoAge algorithms. Cox models were applied to evaluate the risk of dementia. Logistic regression models and linear regression models were used to assess the association between cognitive functions and brain structural measures.
Results: During a median follow-up of 13.68 years, 4744 incident all-cause dementia (ACD) events (including 3013 Alzheimer's disease (AD) and 853 vascular dementia (VaD)) were recorded. Participants with older biological age were at increased risk of incident dementia (HR=1.35, 95% CI 1.23 to 1.48 for KDM-BA acceleration, 1.71 (1.52 to 1.91) for PhenoAge acceleration). Those with the highest level of KDM-BA and PhenoAge acceleration had the highest risk of ACD risk, with the corresponding HR of 1.80 (95% CI 1.60 to 2.03) and 1.19 (1.09 to 1.29), respectively. The associations between biological ageing with AD and VaD were also significant. Furthermore, a higher level of biological age was associated with worse performance in multiple cognitive domains and brain structural measures.
Conclusion: A higher level of biological age may represent a potential risk factor for incident dementia and is associated with worse performance in multiple cognitive domains and brain structural measures.
背景：几项小样本研究表明，衰老的生物学过程与痴呆和认知功能有关。我们的目的是前瞻性地研究生物年龄与痴呆、认知功能和大脑结构之间的关系。方法：共有287846名基线时无痴呆的参与者（随访至2022年11月）进行了分析。我们使用klemera - double法生物年龄（KDM-BA）和PhenoAge算法从临床特征中测量生物年龄。采用Cox模型评估痴呆风险。使用逻辑回归模型和线性回归模型来评估认知功能与大脑结构测量之间的关系。结果：在中位随访13.68年期间，记录了4744例全因痴呆（ACD）事件（包括3013例阿尔茨海默病（AD）和853例血管性痴呆（VaD））。生物年龄较大的参与者发生痴呆的风险增加（HR=1.35， KDM-BA加速的95% CI 1.23至1.48，PhenoAge加速的95% CI 1.71(1.52至1.91)）。KDM-BA和PhenoAge加速水平最高的ACD风险最高，相应的HR分别为1.80 （95% CI 1.60 ~ 2.03）和1.19 （95% CI 1.09 ~ 1.29）。生物老化与AD和VaD之间的关联也很显著。此外，较高的生物年龄水平与多个认知领域和大脑结构测量的较差表现有关。结论：较高的生理年龄水平可能是发生痴呆的潜在危险因素，并且与多个认知领域和大脑结构测量的较差表现有关。
期刊介绍：
Journal of Investigative Medicine (JIM) is the official publication of the American Federation for Medical Research. The journal is peer-reviewed and publishes high-quality original articles and reviews in the areas of basic, clinical, and translational medical research.
JIM publishes on all topics and specialty areas that are critical to the conduct of the entire spectrum of biomedical research: from the translation of clinical observations at the bedside, to basic and animal research to clinical research and the implementation of innovative medical care.
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