Subjective cognitive decline (SCD) has been implicated as an early marker of subtle cognitive change in preclinical Alzheimer’s disease (AD).1 The relationship between SCD and molecular markers of disease progression in AD is poorly understood. Carriers of the presenilin ( PSEN1 E280A) mutation from the Colombian kindred2 are a compelling group in which to study SCD, as they will develop dementia with certainty, and have a well-characterised disease trajectory from presymptomatic to clinical stages.2 SCD has been associated with markers of AD pathology in older adults at risk for late-onset sporadic AD.3 We showed previously that self-reported subjective memory complaints (SMC), a proxy for SCD, were elevated in cognitively unimpaired PSEN1 mutation carriers, and that study-partner-reported SMCs were correlated with age and negatively correlated with hippocampal volume.4 In the present study, we explored the extent to which SCD relates to markers of brain pathology—in vivo amyloid and/or tau. We hypothesised that SCD would be related to neocortical amyloid and regional tau levels. Findings have the potential to inform whether SCD might be a sensitive marker of AD-related pathology and disease trajectory in the preclinical stage of AD. Participants were 21 PSEN1 E280A mutation carriers and 27 age, sex and education-matched non-carrier family members recruited from the Alzheimer’s Prevention Initiative Registry. All had at least one parent who bore the PSEN1 E280A mutation but were blind to their genetic status, in accordance with cultural norms and ethical regulations in this community. Clinical assessments, including neurological exam and psychiatric questionnaires probing depression and anxiety, were completed at the University of Antioquia. SCD was assessed using both the self-report and study-partner-based versions of the Memory Complaint Scale, Spanish version (online supplementary appendix 1). Positron-emission tomography (PET) imaging was done in Boston, Massachusetts, USA. ### Supplementary data [jnnp-2019-321205supp001.pdf] Exclusion criteria included chronic major neurological …

中文翻译：

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临床前常染色体显性阿尔茨海默氏病的主观认知能力下降与脑病理学指标的关联。

主观认知能力下降（SCD）被认为是临床前阿尔茨海默氏病（AD）微妙的认知变化的早期标志物。1人们对SCD与疾病进展的分子标志物之间的关系了解甚少。来自哥伦比亚kindred2的早老素（PSEN1 E280A）突变的携带者是研究SCD的诱人小组，因为它们将确定性地发展为痴呆症，并且具有从症状前到临床阶段的特征明确的疾病轨迹。2与SCD相关带有AD病理学标记物的老年人有迟发性散发性AD的风险。3我们之前曾证明，在没有认知障碍的PSEN1突变携带者中，自我报告的主观记忆障碍（SMC）是SCD的替代物，并且研究伙伴报告的SMC与年龄相关，与海马体积呈负相关。4在本研究中，我们探讨了SCD与脑病理标志物（体内淀粉样蛋白和/或tau蛋白）相关的程度。我们假设SCD与新皮质淀粉样蛋白和区域tau水平有关。这些发现有可能告知SCD是否可能在AD临床前阶段成为与AD相关的病理学和疾病轨迹的敏感标志物。参加者为21个PSEN1 E280A突变携带者，以及从阿尔茨海默氏症预防计划注册中心招募的27个年龄，性别和教育程度匹配的非携带者家庭成员。根据该社区的文化规范和道德规范，所有父母中至少有一位父母患有PSEN1 E280A突变，但对他们的遗传状况视而不见。在安蒂奥基亚大学完成了包括神经系统检查和精神抑郁症问卷在内的临床评估，以探讨抑郁症和焦虑症。使用自我报告和基于研究伙伴的版本的“记忆投诉量表”，西班牙语版本（在线补充附录1）对SCD进行了评估。正电子发射断层扫描（PET）成像在美国马萨诸塞州的波士顿进行。###补充数据[jnnp-2019-321205supp001.pdf]排除标准包括慢性主要神经系统疾病... 正电子发射断层扫描（PET）成像在美国马萨诸塞州的波士顿进行。###补充数据[jnnp-2019-321205supp001.pdf]排除标准包括慢性主要神经系统疾病... 正电子发射断层扫描（PET）成像在美国马萨诸塞州的波士顿进行。###补充数据[jnnp-2019-321205supp001.pdf]排除标准包括慢性主要神经系统疾病...