Department of Medicine, Dalhousie University, Halifax, Canada.
Faculty of Graduate Studies, Dalhousie University, Halifax, Canada.
Int Psychogeriatr. 2021 Oct;33(10):1035-1043. doi: 10.1017/S1041610220003932. Epub 2021 Feb 15.
To examine the relative contributions of frailty and neuropathology to dementia expression in a population-based cohort study.
Cross-sectional analysis of observational data.
Population-representative clinicopathological cohort study.
Adults aged 75+ recruited from general practice registries in Cambridge, UK, in 1985.
A 39-item frailty index and 15-item neuropathological index were used to operationalize frailty and neuropathology, respectively. Dementia status was ascertained by clinical consensus at time of death. Relationships were evaluated using logistic regression models in participants with autopsy records (n = 183). Model fit was assessed using change in deviance. Population attributable fraction for frailty was evaluated in relation to dementia incidence in a representative sample of the survey participants (n = 542).
Participants with autopsy were 92.3 ± 4.6 years at time of death, and mostly women (70%). Average frailty index value at last survey before death was 0.34 ± 0.16. People with dementia (63% of the sample) were frailer, had lower MMSE scores, and a higher burden of neuropathology. Frailty and neuropathological burden were significantly and independently associated with dementia status, without interaction; frailty explained an additional 3% of the variance in the model. Assuming a causal relationship and based on population-attributable fraction analyses, preventing severe frailty (Frailty Index ≥ 0.40) could have avoided 14.2% of dementia cases in this population-based cohort.
In the very old, frailty contributes to the risk for dementia beyond its relationship with the burden of traditional dementia neuropathologies. Reducing frailty could have important implications for controlling the burden of dementia. Future research on frailty interventions should include dementia risk as a key outcome, public health interventions and policy decisions should consider frailty as a key risk factor for dementia, and biomedical research should focus on elucidating shared mechanisms of frailty and dementia development.
在一项基于人群的队列研究中，研究衰弱和神经病理学对痴呆表现的相对贡献。
观察性数据的横断面分析。
具有代表性的人群临床病理队列研究。
1985 年从英国剑桥的普通实践登记处招募的 75 岁及以上成年人。
使用 39 项衰弱指数和 15 项神经病理学指数分别对衰弱和神经病理学进行操作化。痴呆状态通过死亡时的临床共识确定。在有尸检记录的参与者中（n = 183），使用逻辑回归模型评估了这些关系。使用偏差的变化评估模型拟合度。在调查参与者的代表性样本中（n = 542），评估衰弱的人群归因分数与痴呆发生率的关系。
有尸检记录的参与者在死亡时的年龄为 92.3 ± 4.6 岁，大多数为女性（70%）。死亡前最后一次调查时的平均衰弱指数值为 0.34 ± 0.16。患有痴呆症（占样本的 63%）的人更虚弱，MMSE 评分更低，神经病理学负担更高。衰弱和神经病理学负担与痴呆状态显著且独立相关，没有相互作用；衰弱在模型中解释了额外的 3%的方差。基于人群归因分数分析，假设因果关系，预防严重衰弱（衰弱指数≥0.40）可以避免该人群中 14.2%的痴呆病例。
在非常老的人群中，衰弱除了与传统痴呆神经病理学负担有关外，还会增加痴呆的风险。减少衰弱可能对控制痴呆负担具有重要意义。关于衰弱干预的未来研究应将痴呆风险作为关键结果，公共卫生干预和政策决策应将衰弱视为痴呆的关键风险因素，生物医学研究应重点阐明衰弱和痴呆发展的共同机制。
