University of Bordeaux, CNRS, UMR 5293, Institut des Maladies Neurodégénératives, France (G.P., L.N., B.M., V.P.).
Centre Mémoire de Ressources et de Recherches, Pôle de Neurosciences Cliniques, CHU de Bordeaux, France (G.P., L.N., J.-F.D., V.P.).
Stroke. 2021 May;52(5):1741-1750. doi: 10.1161/STROKEAHA.120.031743. Epub 2021 Mar 4.
Many neurological or psychiatric diseases affect the hippocampus during aging. The study of hippocampal regional vulnerability may provide important insights into the pathophysiological mechanisms underlying these processes; however, little is known about the specific impact of vascular brain damage on hippocampal subfields atrophy.
To analyze the effect of vascular injuries independently of other pathological conditions, we studied a population-based cohort of nondemented older adults, after the exclusion of people who were diagnosed with neurodegenerative diseases during the 14-year clinical follow-up period. Using an automated segmentation pipeline, 1.5T-magnetic resonance imaging at inclusion and 4 years later were assessed to measure both white matter hyperintensities and hippocampal subfields volume. Annualized rates of white matter hyperintensity progression and annualized rates of hippocampal subfields atrophy were then estimated in each participant.
We included 249 participants in our analyses (58% women, mean age 71.8, median Mini-Mental State Evaluation 29). The volume of the subiculum at baseline was the only hippocampal subfield volume associated with total, deep/subcortical, and periventricular white matter hyperintensity volumes, independently of demographic variables and vascular risk factors (β=-0.17, =0.011; β=-0.25, =0.020 and β=-0.14, =0.029, respectively). In longitudinal measures, the annualized rate of subiculum atrophy was significantly higher in people with the highest rate of deep/subcortical white matter hyperintensity progression, independently of confounding factors (β=-0.32, =0.014).
These cross-sectional and longitudinal findings highlight the links between vascular brain injuries and a differential vulnerability of the subiculum within the hippocampal loop, unbiased of the effect of neurodegenerative diseases, and particularly when vascular injuries affect deep/subcortical structures.
许多神经或精神疾病在衰老过程中会影响海马体。研究海马区域易损性可能为这些过程的病理生理机制提供重要的见解；然而，关于血管性脑损伤对海马亚区萎缩的具体影响知之甚少。
为了独立于其他病理情况分析血管损伤的影响，我们研究了一个基于人群的非痴呆老年队列，在排除了在 14 年临床随访期间被诊断为神经退行性疾病的人群后。使用自动分割管道，在纳入时和 4 年后进行 1.5T 磁共振成像，以测量白质高信号和海马亚区体积。然后在每个参与者中估计白质高信号进展的年增长率和海马亚区萎缩的年增长率。
我们在分析中纳入了 249 名参与者（58%为女性，平均年龄 71.8 岁，中位数简易精神状态评估 29 分）。基线时的下托区体积是唯一与总白质高信号、深部/皮质下白质高信号和脑室周围白质高信号体积相关的海马亚区体积，独立于人口统计学变量和血管危险因素（β=-0.17，P=0.011；β=-0.25，P=0.020 和β=-0.14，P=0.029）。在纵向测量中，深部/皮质下白质高信号进展最快的人的下托区萎缩年增长率显著更高，独立于混杂因素（β=-0.32，P=0.014）。
这些横断面和纵向研究结果强调了血管性脑损伤与海马环路中下托区易损性之间的联系，不受神经退行性疾病影响，特别是当血管损伤影响深部/皮质下结构时。
