青年期血管危险因素与中年脑老化标志的关联
基于 CARDIA 前瞻性队列的长程认知与神经影像数据，识别中年认知下降相关的青年期血管危险因素和脑结构改变特征。结果显示，40 岁前较高的收缩压和吸烟是中年认知轨迹分组的关键预测因素。认知下降组表现出白质高信号加速积累、额颞叶及丘脑灰质体积改变和以基底前脑为中心的网络重组。
要点
- 40 岁前可能是管理血管危险因素以保护中年认知的关键窗口。
- 青年期收缩压升高和吸烟与中年认知下降相关。
- 白质高信号和灰质改变提示血管因素可同时驱动脑血管与神经退行性损伤。
核心结论
- 40 岁前可能是管理血管危险因素、保护中年认知的关键时间窗口。
- 白质高信号和灰质改变并存提示血管因素可同时驱动脑血管损伤和神经退行性损伤。
- 以基底前脑为中心的神经影像特征可能反映早期血管应激后的胆碱能与胶质反应。
研究设计与样本
- 利用 CARDIA 前瞻性队列 1985—2020 年共 35 年的血管危险因素、认知和神经影像纵向数据。
- 对认知轨迹进行 K 均值聚类，识别下降组与稳定组。
- 在 720 名平均年龄 61±3.5 岁的参与者中重复检验青年期收缩压分层与中年认知表现的关联。
主要发现
- 在 280 名有纵向数据的参与者中，40 岁前较高的收缩压和吸烟是中年认知分组的关键因素，特征重要性分别约为 0.3 和 0.2。
- 认知下降组与稳定组在白质高信号积累、额叶和颞叶联合皮质、枕极和丘脑灰质体积变化上存在差异，β 范围为 –0.0006 至 –0.002，P≤0.02。
- 认知下降组表现出以基底前脑为中心、跨越早年至中年晚期的脑网络水平重组。
- 在 720 名参与者中，青年期收缩压分层与中年认知表现呈阶梯式剂量依赖性关联。
- 280 名纵向数据参与者基线平均年龄为 50±3.5 岁，女性占 52% 至 56%，黑人占 40% 至 41%，中位随访 10 年。
关键数值与推荐
- 40 岁前作为关键时间窗口的定义来自 CARDIA 研究中青年期收缩压分层与中年认知的关联。
- 白质高信号、灰质体积和网络重组差异来自认知轨迹下降组与稳定组的比较。
临床怎么用
- 临床可考虑在 40 岁前加强收缩压控制和戒烟干预以保护中年认知功能。
- 白质高信号和以基底前脑为中心的网络改变可能作为中年认知下降的影像监测指标。
以上解读依据论文摘要（全文未开放获取或许可不允许翻译转载）。
原文
Stroke, Volume 57, Issue 10, Page 3055-3068, October 1, 2026. BACKGROUND:Early-life vascular risk factors are increasingly linked to midlife cognitive decline, though critical risk periods remain unclear. These factors also relate to structural brain changes, yet midlife alterations tied to cognitive decline are poorly defined. We leveraged data from the CARDIA study (Coronary Artery Risk Development in Young Adults) to identify critical periods and factors associated with midlife cognition and neuroimaging signatures.METHODS:We utilized longitudinal cognitive and neuroimaging data from the prospective CARDIA study with vascular risk factor data spanning 35 years (1985–2020). K-means clustering of cognitive trajectories identified Declined and Stable clusters. A gradient boosting classifier identified factors predictive of cluster membership. Linear mixed-effects models assessed cluster differences in structural brain changes, and structural covariance analyses identified brain network remodeling linked to cognitive decline. Cross-sectional late-midlife cognitive data were used to examine associations between early adulthood (ages 18–40 years) systolic blood pressure strata and cognitive outcomes.RESULTS:Among 280 participants with longitudinal data (mean age, 50±3.5 years at baseline; 52% to 56% female, 40% to 41% Black race) followed for a median of 10 years, higher systolic blood pressure and smoking before age 40 years were critical factors for cognitive cluster membership in late midlife (feature importance ≈0.3 and 0.2, respectively). Accelerated accumulation of white matter hyperintensities, gray matter volume changes involving frontal and temporal association cortices, occipital pole and thalamus (β range, –0.0006 to –0.002;P≤0.02), and network-level reorganization predominantly involving the basal forebrain spanning early- to late-midlife distinguished clusters. A stepwise, dose-dependent association between early-life systolic blood pressure strata and late-midlife cognitive performance was replicated in 720 participants (mean age, 61±3.5 years).CONCLUSIONS:Before age 40 years may be a critical window to manage vascular risk factors and preserve midlife cognition. Linked white matter hyperintensity and gray matter changes suggest that vascular factors drive both cerebrovascular and neurodegenerative injury. A basal forebrain–centered neuroimaging signature, possibly reflecting cholinergic and glial responses to early vascular stress, may serve as
引用
- Stroke：Early Life Vascular Risk and Midlife Markers of Brain Aging
供执业医师工作参考，不替代临床判断；数值与分级以指南原文为准。