Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD, 21205.
Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, 21287.
Ann Clin Transl Neurol. 2020 Aug;7(8):1307-1317. doi: 10.1002/acn3.51120. Epub 2020 Jul 21.
Examine whether cognitive reserve moderates the association of 1) vascular risk factors and 2) white matter hyperintensity burden with risk of clinical progression and longitudinal cognitive decline.
BIOCARD Study participants were cognitively normal and primarily middle-aged (M = 57 years) at baseline and have been followed with annual cognitive and clinical assessments (M = 13 years). Baseline cognitive reserve was indexed with a composite score combining education with reading and vocabulary scores. Baseline vascular risk (N = 229) was assessed with a composite risk score reflecting five vascular risk factors. Baseline white matter hyperintensity load (N = 271) was measured with FLAIR magnetic resonance imaging. Cox regression models assessed risk of progression from normal cognition to onset of clinical symptoms of Mild Cognitive Impairment. Longitudinal mixed effects models measured the relationship of these variables to cognitive decline, using a global composite score, and executive function and episodic memory sub-scores.
Both vascular risk and white matter hyperintensities were associated with cognitive decline, particularly in executive function. Higher vascular risk, but not white matter hyperintensity burden, was associated with an increased risk of progression to Mild Cognitive Impairment. Higher cognitive reserve was associated with a reduced risk of symptom onset and higher levels of baseline cognition but did not modify the associations between the vascular risk score and white matter hyperintensities with clinical progression or cognitive decline.
Although cognitive reserve has protective effects on clinical and cognitive outcomes, it does not mitigate the negative impact of vascular risk and small vessel cerebrovascular disease on these same outcomes.
探讨认知储备是否调节以下两者与临床进展和纵向认知衰退的关联：1）血管危险因素；2）脑白质高信号负担。
BIOCARD 研究的参与者在基线时认知正常，主要为中年（平均年龄 57 岁），并接受了每年一次的认知和临床评估（平均随访 13 年）。基线认知储备用教育程度与阅读和词汇得分的综合评分来表示。基线血管风险（N=229）用反映五种血管危险因素的综合风险评分来评估。基线脑白质高信号负荷（N=271）用 FLAIR 磁共振成像来测量。Cox 回归模型评估了从正常认知进展到出现轻度认知障碍临床症状的风险。纵向混合效应模型使用全球综合评分以及执行功能和情景记忆子评分，评估这些变量与认知衰退的关系。
血管风险和脑白质高信号均与认知衰退有关，尤其是在执行功能方面。较高的血管风险，但不是脑白质高信号负荷，与向轻度认知障碍进展的风险增加有关。较高的认知储备与症状发作风险降低和基线认知水平升高有关，但不能改变血管风险评分与脑白质高信号与临床进展或认知衰退之间的关联。
尽管认知储备对临床和认知结局有保护作用，但它不能减轻血管风险和小血管脑血管病对这些结局的负面影响。
