Vogel Jacob W, Varga Doležalová Monika, La Joie Renaud, Marks Shawn M, Schwimmer Henry D, Landau Susan M, Jagust William J
From Helen Wills Neuroscience Institute (J.W.V., M.V.D., R.L.J., S.M.M., H.D.S., S.M.L., W.J.J.), University of California, Berkeley; and Memory and Aging Center (R.L.J.), University of California, San Francisco.
Neurology. 2017 Nov 7;89(19):2002-2009. doi: 10.1212/WNL.0000000000004627. Epub 2017 Oct 6.
To assess in a longitudinal study whether subjective cognitive decline (SCD) and brain β-amyloid (Aβ) contribute unique information to cognitive decline.
One hundred thirty-six healthy elderly from the Berkeley Aging Cohort Study were followed up for a mean of 4 years. SCD and affective measures were generated from the Geriatric Depression Scale (GDS) with factor analysis on data from a larger set of 347 healthy, nondepressed (GDS <11) elderly individuals. Cognition was summarized with previously validated factor scores. Pittsburgh compound B (PiB)-PET scans were acquired to determine the presence (PiB+) or absence (PiB-) of Aβ pathology. Mixed models were used to assess the independent and interactive effects of SCD, affective features, PiB status, and time on cognition, with adjustment for demographic variables.
SCD score demonstrated good construct validity compared to an existing measure of subjective memory and was partially explained by several lower-order measurements. Mixed models revealed that SCD interacted with PiB status to predict change in episodic memory and global cognition over time, with adjustment for affective features. PiB+ individuals with more severe SCD demonstrated the steepest cognitive decline. Worse SCD predicted faster decline in working memory independently of PiB status. No such effects were seen for affective scores when adjusted for SCD.
PiB+ individuals with SCD are at greatest risk of cognitive decline. Evidence for amyloid alone is not sufficient to indicate risk of rapid cognitive decline in healthy elderly. Effects of GDS on cognitive decline in nondepressed cohorts may be driven by SCD rather than subsyndromal depression.
在一项纵向研究中评估主观认知下降（SCD）和脑β-淀粉样蛋白（Aβ）是否为认知下降提供独特信息。
对来自伯克利衰老队列研究的136名健康老年人进行了平均4年的随访。SCD和情感测量数据来自老年抑郁量表（GDS），并对来自347名健康、无抑郁（GDS<11）老年人的更大数据集进行了因子分析。认知情况用先前验证的因子得分进行总结。通过匹兹堡化合物B（PiB）-PET扫描来确定是否存在Aβ病理（PiB+）或不存在（PiB-）。使用混合模型评估SCD、情感特征、PiB状态和时间对认知的独立和交互作用，并对人口统计学变量进行调整。
与现有的主观记忆测量方法相比，SCD评分显示出良好的结构效度，并且部分由几个低阶测量指标解释。混合模型显示，在对情感特征进行调整后，SCD与PiB状态相互作用，可预测随时间推移情景记忆和整体认知的变化。SCD更严重的PiB+个体认知下降最为明显。较差的SCD独立于PiB状态可预测工作记忆下降更快。在对SCD进行调整后，情感评分未显示出此类影响。
患有SCD的PiB+个体认知下降风险最大。仅淀粉样蛋白的证据不足以表明健康老年人快速认知下降的风险。在无抑郁队列中，GDS对认知下降的影响可能由SCD而非亚综合征性抑郁驱动。
