I read with great interest the recent study by Startin et al. [1] demonstrating a clinical trial model for evaluation of preclinical and prodromal cognition marker in Down syndrome (DS) associated with Alzheimer’s disease (AD)-linked dementia [1]. This significant study has measured age group effect size for a randomized clinical trial (RCT) on DS (N 5 297) by h2 values from cognition test measures, including simple reaction time (SRT), paired associates learning (PAL), and objectmemory [1]. Comparedwith reference 16-30 years age DS group, significantly poor cognition was observed among people grouped in 41-45 years age DS group (N5 24). People grouped in 46-50 years age DS group (N 5 24) showed significantly low performance for most of the cognition measures. The DS individuals with prodromal dementia (N 5 46/170) perform significantly poor in cognition measures (variance in scores5.12%) when compared with DS with preclinical dementia (N5 68/170), and the effect is more apparent (variance in scores5. 20%) between DSwith clinical dementia (N5 56/170) andDSwith preclinical dementia (N5 68/170) [1]. In this study, Startin et al. used PAL first trial memory score as a primary outcome measure, counting a minimum of 43 individuals with DS in 36-40 year age group, for clinical trial testing treatment (with 90% significance) effect on delay in early cognition decline [1]. The adaptive behavior score total (ABST) counts 56 and 36 samples for DS in 46-50 and 51-55 age groups, respectively, required in aRCT for testing the effect of intervention delaying cognition decline [1]. Appreciably, the study design is unique and involved countermeasures, and modeling scores from primary outcome measure score for counting sample size in RCT is a path-leading research. However, it is not explicit which patients with DS included in this study already had AD. Why are there two different outcome measure scores for effect size calculations, the PAL first trial memory score for 36-40 year age group versus ABST score

中文翻译：

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唐氏综合征认知标志物在阿尔茨海默病和痴呆管理中的意义

我非常感兴趣地阅读了 Startin 等人最近的研究。[1] 展示了一种临床试验模型，用于评估与阿尔茨海默病 (AD) 相关的痴呆症相关的唐氏综合征 (DS) 的临床前和前驱认知标志物 [1]。这项重要研究通过认知测试测量的 h2 值测量了 DS (N 5 297) 随机临床试验 (RCT) 的年龄组效应大小，包括简单反应时间 (SRT)、配对关联学习 (PAL) 和对象记忆。 1]。与参考16-30岁DS组相比，41-45岁DS组(N5 24)的人群认知显着较差。分组在 46-50 岁 DS 组 (N 5 24) 的人在大多数认知测量中表现出显着的低表现。与临床前痴呆的 DS (N5 68/170) 相比，前驱性痴呆 (N 5 46/170) 的 DS 个体在认知测量方面的表现明显较差（得分差异为 5.12%），并且效果更明显（差异为评分 5. 20%) 的临床痴呆 (N5 56/170) 和临床前痴呆 (N5 68/170) [1]。在这项研究中，Startin 等人。使用 PAL 首次试验记忆评分作为主要结果衡量指标，对 36-40 岁年龄组的至少 43 名 DS 患者进行计数，用于临床试验测试治疗（具有 90% 显着性）对延迟早期认知衰退的影响 [1]。适应性行为总分 (ABST) 分别为 46-50 和 51-55 岁年龄组的 DS 计数了 56 和 36 个样本，这是 aRCT 测试延迟认知衰退干预效果所需的 [1]。可观地，该研究设计独特且涉及对策，并且从主要结果测量得分建模得分以计算 RCT 中的样本量是一项领先的研究。然而，尚不清楚本研究中哪些 DS 患者已经患有 AD。为什么效果大小计算有两种不同的结果测量分数，36-40 岁年龄组的 PAL 首次试验记忆分数与 ABST 分数