Yushun Yan, Hailin Xiang, Min Wang, Jinxue Wei, Huanhuan Fan, Yue Du, Yuanmei Tao, Yikai Dou, Yangrui Ma, Xiao Yang, Xiaohong Ma
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Addictive and multiplicative interactions were calculated to evaluate the synergistic effect. A total of 64,706 participants were included at baseline (mean age: 63.9, female: 55.2%), where 4197 (6.5%) individuals had depressive symptoms only, 28,175 (43.5%) individuals had cognitive impairment only, 11,564 (17.9%) individuals had both, and 20,770 (32.1%) individuals had neither. Compared with the neither group, all the other three groups had higher risks of subsequent dementia (depression only: HR 1.65, 95% CI 1.26-2.17; cognitive impairment only: HR 2.71, 95% CI 2.33-3.14; depression with cognitive impairment: HR 3.51, 95% CI 2.95-4.17). There was insignificant additive (RERI, 0.15, 95% CI -0.45-0.75; AP, 0.042, 95% CI -0.13-0.21; SI, 1.06, 95% CI 0.83-1.37) and multiplicative (0.78, 95% CI 0.58-1.06) interaction between depression and cognitive impairment on subsequent dementia. 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引用次数: 0
摘要
抑郁症通常伴有认知障碍,会增加罹患痴呆症的风险。然而,关于抑郁症与认知障碍的效应大小以及它们对未来痴呆症的协同效应的证据还很有限。为了探讨这一问题,我们研究了三个大型跨国人群前瞻性队列。抑郁症状通过流行病学量表进行评估,认知障碍则通过主观认知测试进行界定。痴呆症通过自我报告的医生诊断情况来确定。在对潜在混杂变量进行调整后,采用 Cox 比例危险模型确定危险比(HR)和 95% 置信区间(95% CI)。计算了成瘾性和乘法交互作用,以评估协同效应。基线研究共纳入 64706 名参与者(平均年龄:63.9 岁,女性:55.2%),其中 4197 人(6.5%)仅有抑郁症状,28175 人(43.5%)仅有认知障碍,11564 人(17.9%)两者都有,20770 人(32.1%)两者都没有。与两组均无痴呆症的患者相比,其他三组患者罹患痴呆症的风险都更高(仅有抑郁症:HR 1.65,95% CI 1.26-2.17;仅有认知障碍:HR 2.71,95% CI 2.33-3.14;抑郁症伴有认知障碍:HR 3.51,95% CI 2.33-3.14):HR 3.51,95% CI 2.95-4.17)。抑郁症和认知障碍对继发性痴呆的交互作用不显著(RERI, 0.15, 95% CI -0.45-0.75;AP, 0.042, 95% CI -0.13-0.21;SI, 1.06, 95% CI 0.83-1.37),而两者之间的交互作用是相乘的(0.78, 95% CI 0.58-1.06)。我们发现,抑郁症合并认知障碍的痴呆症风险高于单独两种情况,这两种因素之间不存在显著的协同效应。
Effects of depression and cognitive impairment on increased risks of incident dementia: a prospective study from three elderly cohorts.
Depression is usually accompanied with cognitive impairment and increases risk of incident dementia. However, evidence has been limited on the effect size of depression with cognitive impairment and their synergistic effect on future dementia. To explore this, we examined three large cross-country population-based prospective cohorts. Depressive symptoms were assessed by epidemiologic scale, while cognitive impairment was defined by subjective cognitive tests. Dementia was ascertained by self-reported physician-diagnosed conditions. Cox proportional hazard models were employed to determine the hazard ratio (HR) and 95% confidence interval (95% CI), with adjustments of potential confounding variables. Addictive and multiplicative interactions were calculated to evaluate the synergistic effect. A total of 64,706 participants were included at baseline (mean age: 63.9, female: 55.2%), where 4197 (6.5%) individuals had depressive symptoms only, 28,175 (43.5%) individuals had cognitive impairment only, 11,564 (17.9%) individuals had both, and 20,770 (32.1%) individuals had neither. Compared with the neither group, all the other three groups had higher risks of subsequent dementia (depression only: HR 1.65, 95% CI 1.26-2.17; cognitive impairment only: HR 2.71, 95% CI 2.33-3.14; depression with cognitive impairment: HR 3.51, 95% CI 2.95-4.17). There was insignificant additive (RERI, 0.15, 95% CI -0.45-0.75; AP, 0.042, 95% CI -0.13-0.21; SI, 1.06, 95% CI 0.83-1.37) and multiplicative (0.78, 95% CI 0.58-1.06) interaction between depression and cognitive impairment on subsequent dementia. We found depression with cognitive impairment has higher risks of dementia than either condition alone and no significant synergistic effect exists between these two factors.
期刊介绍:
Psychiatry has suffered tremendously by the limited translational pipeline. Nobel laureate Julius Axelrod''s discovery in 1961 of monoamine reuptake by pre-synaptic neurons still forms the basis of contemporary antidepressant treatment. There is a grievous gap between the explosion of knowledge in neuroscience and conceptually novel treatments for our patients. Translational Psychiatry bridges this gap by fostering and highlighting the pathway from discovery to clinical applications, healthcare and global health. We view translation broadly as the full spectrum of work that marks the pathway from discovery to global health, inclusive. The steps of translation that are within the scope of Translational Psychiatry include (i) fundamental discovery, (ii) bench to bedside, (iii) bedside to clinical applications (clinical trials), (iv) translation to policy and health care guidelines, (v) assessment of health policy and usage, and (vi) global health. All areas of medical research, including — but not restricted to — molecular biology, genetics, pharmacology, imaging and epidemiology are welcome as they contribute to enhance the field of translational psychiatry.