Newman Benjamin T, Danoff Joshua S, Lynch Morgan E, Giamberardino Stephanie N, Gregory Simon G, Connelly Jessica J, Druzgal T Jason, Morris James P
Department of Psychology, University of Virginia, Charlottesville, Virginia, USA.
Department of Radiology and Medical Imaging, School of Medicine, University of Virginia, Charlottesville, Virginia, USA.
Aging Cell. 2025 Apr;24(4):e14426. doi: 10.1111/acel.14426. Epub 2024 Nov 28.
Epigenetic clocks provide powerful tools for estimating health and lifespan but their ability to predict brain degeneration and neuronal damage during the aging process is unknown. In this study, we use GrimAge, an epigenetic clock correlated to several blood plasma proteins, to longitudinally investigate brain cellular microstructure in axonal white matter from a cohort of healthy aging individuals. A specific focus was made on white matter hyperintensities, a visible neurological manifestation of small vessel disease, and the axonal pathways throughout each individual's brain affected by their unique white matter hyperintensity location and volume. 98 subjects over 55 years of age were scanned at baseline with 41 returning for a follow-up scan 2 years later. Using diffusion MRI lesionometry, we reconstructed subject-specific networks of affected axonal tracts and examined the diffusion cellular microstructure composition of these areas, both at baseline and longitudinally, for evidence of cellular degeneration. A chronological age-adjusted version of GrimAge was significantly correlated with baseline WMH volume and markers of neuronal decline, indicated by increased extracellular free water, increased intracellular signal, and decreased axonal signal within WMH. By isolating subject-specific axonal regions "lesioned" by crossing through a WMH, age-adjusted GrimAge was also able to predict longitudinal development of similar patterns of neuronal decline throughout the brain. This study is the first to demonstrate WMH lesionometry as a subject-specific precision imaging technique to study degeneration in aging and the first to establish a relationship between accelerated epigenetic GrimAge and brain cellular microstructure in humans.
表观遗传时钟为评估健康状况和寿命提供了强大的工具,但其在衰老过程中预测脑退化和神经元损伤的能力尚不清楚。在本研究中,我们使用与几种血浆蛋白相关的表观遗传时钟GrimAge,对一组健康衰老个体轴突白质中的脑细胞微观结构进行纵向研究。特别关注了白质高信号,这是小血管疾病的一种可见神经学表现,以及受个体独特的白质高信号位置和体积影响的贯穿每个人大脑的轴突通路。98名55岁以上的受试者在基线时进行了扫描,其中41人在两年后返回进行随访扫描。使用扩散磁共振成像病变测量法,我们重建了受影响轴突束的个体特异性网络,并在基线和纵向检查了这些区域的扩散细胞微观结构组成,以寻找细胞退化的证据。GrimAge的按时间年龄调整版本与基线白质高信号体积和神经元衰退标志物显著相关,白质高信号内细胞外自由水增加、细胞内信号增加和轴突信号减少表明了这一点。通过分离因穿过白质高信号而“受损”的个体特异性轴突区域,按年龄调整的GrimAge还能够预测整个大脑中类似神经元衰退模式的纵向发展。本研究首次证明白质高信号病变测量法是一种用于研究衰老过程中退化的个体特异性精确成像技术,也是首次在人类中建立加速表观遗传GrimAge与脑细胞微观结构之间的关系。