Soldan Anja, Pettigrew Corinne, Cai Qing, Wang Jiangxia, Wang Mei-Cheng, Moghekar Abhay, Miller Michael I, Albert Marilyn
Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Neurobiol Aging. 2017 Dec;60:164-172. doi: 10.1016/j.neurobiolaging.2017.09.002. Epub 2017 Sep 11.
We examined if baseline levels of cognitive reserve (CR) and of Alzheimer's disease (AD) biomarkers modify the rate of change in cognition among individuals with normal cognition at baseline (n = 303, mean baseline age = 57 years, mean follow-up = 12 years); 66 participants subsequently developed mild cognitive impairment (MCI) or dementia due to AD. CR was indexed by years of education, reading, and vocabulary measures. AD biomarkers were measured with a composite score composed of measures of amyloid, phosphorylated tau, and neurodegeneration. Higher CR scores were associated with better cognitive performance but did not modify the rate of change in cognition among those who remained cognitively normal, nor among those who progressed to MCI before symptom onset, independent of baseline biomarker levels. However, higher CR scores were associated with faster cognitive decline after symptom onset of MCI. These results suggest that the mechanism by which CR mediates the relationship between pathology and cognitive function is by delaying the onset of symptoms rather than reducing the rate of cognitive decline.
我们研究了认知储备（CR）和阿尔茨海默病（AD）生物标志物的基线水平是否会改变基线认知正常个体（n = 303，平均基线年龄 = 57岁，平均随访时间 = 12年）的认知变化率；66名参与者随后因AD发展为轻度认知障碍（MCI）或痴呆。CR通过教育年限、阅读和词汇量测量进行索引。AD生物标志物通过由淀粉样蛋白、磷酸化tau蛋白和神经变性测量组成的综合评分来测量。较高的CR评分与较好的认知表现相关，但在认知保持正常的人群中，以及在症状出现前进展为MCI的人群中，均未改变认知变化率，且与基线生物标志物水平无关。然而，较高的CR评分与MCI症状出现后更快的认知衰退相关。这些结果表明，CR介导病理与认知功能之间关系的机制是通过延迟症状发作，而非降低认知衰退率。
