Stroke Prevention and Atherosclerosis Research Centre, Robarts Research Institute, Western University, London, Ontario, Canada; Department of Clinical Neurological Sciences, Western University, London, ON, Canada; Department of Epidemiology and Biostatistics, Schulich School of Medicine & Dentistry, Western University, London, Ontario, Canada; Department of Neurology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Department of Neurology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Ageing Res Rev. 2020 Mar;58:101002. doi: 10.1016/j.arr.2019.101002. Epub 2019 Dec 30.
This systematic review and meta-analysis assessed the bidirectional association between AD pathology and dementia in community-dwelling elderly populations. We searched PubMed/MEDLINE, Embase, Scopus, Web of Science, and references of the pertinent articles for community/population-based longitudinal cohorts with regular assessment of cognitive status of participants followed by postmortem neuropathology data, with no language and date restrictions, until 20 September 2019. Finally, we retrieved 18 articles with data from 17 cohorts comprising 4677 persons. Dementia was twice as likely in participants with definitive neuropathological indicator for AD compared to those without it: moderate/high Braak and Braak (BB) stages III-VI of neurofibrillary tangles (54 % vs. 26 % in participants with BB stages 0-II), the Consortium to Establish a Registry for AD (CERAD) moderate/frequent neuritic plaques scores (64 % vs. 33 % in participants with CERAD none/infrequent), and National Institute on Aging and the Reagan Institute of the Alzheimer's Association criteria intermediate/high AD probability (52 % vs. 28 % in participants with no/low AD probability). Accordingly, a substantial proportion of community-dwelling elderly people with definitive AD pathology may not develop dementia. Brain reserve or contribution of other factors and pathologies, such as vascular and degenerative pathology to dementia might explain this apparent discrepancy. These findings also suggest caution in equating Alzheimer pathology biomarkers with dementia.
本系统评价和荟萃分析评估了社区居住的老年人中 AD 病理与痴呆之间的双向关联。我们检索了 PubMed/MEDLINE、Embase、Scopus、Web of Science 和相关文章的参考文献，纳入了对参与者认知状态进行定期评估、并随后进行尸检神经病理学数据的社区/人群为基础的纵向队列研究，无语言和日期限制，检索时间截至 2019 年 9 月 20 日。最终，我们检索到 18 篇文章，这些文章的数据来自包含 4677 人的 17 个队列。与没有 AD 神经病理学指标的参与者相比，具有明确 AD 神经病理学指标的参与者发生痴呆的可能性是其两倍：中度/高度 Braak 和 Braak（BB）神经原纤维缠结分期 III-VI（BB 分期 0-II 期参与者中 54% vs. 26%）、认知障碍症建立登记册联合会（CERAD）中度/频繁神经原纤维缠结评分（CERAD 无/不频繁参与者中 64% vs. 33%）和美国国家老龄化研究所和里根协会阿尔茨海默病协会标准中度/高 AD 可能性（无/低 AD 可能性参与者中 52% vs. 28%）。因此，相当一部分患有明确 AD 病理的社区居住老年人可能不会发展为痴呆。大脑储备或其他因素和病理学（如血管和退行性病理学）对痴呆的贡献可能解释了这一明显差异。这些发现还表明，将阿尔茨海默病病理生物标志物等同于痴呆时需要谨慎。
