Department of Psychiatry New York University (NYU) Grossman School of Medicine New York NY.
VA Boston Cooperative Studies ProgramMAVERICVA Boston Healthcare System Boston MA.
J Am Heart Assoc. 2022 May 3;11(9):e023918. doi: 10.1161/JAHA.121.023918. Epub 2022 Apr 26.
Background Vascular function is compromised in Alzheimer disease (AD) years before amyloid and tau pathology are detected and a substantial body of work shows abnormal platelet activation states in patients with AD. The aim of our study was to investigate whether platelet function in middle age is independently associated with future risk of AD. Methods and Results We examined associations of baseline platelet function with incident dementia risk in the community-based FHS (Framingham Heart Study) longitudinal cohorts. The association between platelet function and risk of dementia was evaluated using the cumulative incidence function and inverse probability weighted Cox proportional cause-specific hazards regression models, with adjustment for demographic and clinical covariates. Platelet aggregation response was measured by light transmission aggregometry. The final study sample included 1847 FHS participants (average age, 53.0 years; 57.5% women). During follow-up (median, 20.5 years), we observed 154 cases of incident dementia, of which 121 were AD cases. Results from weighted models indicated that platelet aggregation response to adenosine diphosphate 1.0 µmol/L was independently and positively associated with dementia risk, and it was preceded in importance only by age and hypertension. Sensitivity analyses showed associations with the same directionality for participants defined as adenosine diphosphate hyper-responders, as well as the platelet response to 0.1 µmol/L epinephrine. Conclusions Our study shows individuals free of antiplatelet therapy with a higher platelet response are at higher risk of dementia in late life during a 20-year follow-up, reinforcing the role of platelet function in AD risk. This suggests that platelet phenotypes may be associated with the rate of dementia and potentially have prognostic value.
血管功能在阿尔茨海默病(AD)患者出现淀粉样蛋白和 tau 病理改变之前多年就已经受损,大量研究表明 AD 患者存在血小板激活状态异常。我们的研究旨在探讨中年血小板功能是否与 AD 的未来发病风险独立相关。
我们在基于社区的弗雷明汉心脏研究(Framingham Heart Study)纵向队列中,检查了基线血小板功能与痴呆发病风险之间的关联。使用累积发病率函数和逆概率加权 Cox 比例病因特定风险回归模型评估血小板功能与痴呆风险之间的关系,调整了人口统计学和临床协变量。通过透光比浊法测量血小板聚集反应。最终研究样本包括 1847 名 FHS 参与者(平均年龄 53.0 岁;57.5%为女性)。在随访期间(中位数为 20.5 年),我们观察到 154 例新发痴呆病例,其中 121 例为 AD 病例。加权模型的结果表明,对 1.0 μmol/L 二磷酸腺苷的血小板聚集反应与痴呆风险独立且呈正相关,其重要性仅次于年龄和高血压。敏感性分析显示,对于被定义为二磷酸腺苷高反应者的参与者,以及对 0.1 μmol/L 肾上腺素的血小板反应,均存在相同方向的关联。
我们的研究表明,在 20 年的随访期间,无抗血小板治疗且血小板反应较高的个体在晚年患痴呆的风险更高,这强化了血小板功能在 AD 风险中的作用。这表明血小板表型可能与痴呆的发生速度有关,并且具有潜在的预后价值。