Lee Ji Han, Ryan John, Andreescu Carmen, Aizenstein Howard, Lim Hyun Kook
aWashington University, St Louis, Missouri bDepartment of Psychiatry, School of Medicine, The University of Pittsburgh, Pittsburgh, Pennsylvania, USA cDepartment of Psychiatry, The Saint Vincent Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Neuroreport. 2015 May 6;26(7):411-5. doi: 10.1097/WNR.0000000000000362.
As brainstem nuclei are interconnected with several cortical structures and regulate several autonomic, cognitive, and behavioral functions, it might be important to place the brainstem within an important pathologic core in the progression of Alzheimer's disease (AD). Although there have been several postmortem studies reporting neuropathological alterations of the brainstem in AD, there has been no in-vivo structural neuroimaging study of the brainstem in the patients with AD. The aim of this study was to investigate differences in the brainstem volume and shape between patients with AD and elderly normal controls. Fifty AD patients (the Clinical Dementia Rating Scale ≥ 1) and 50 normal controls were recruited, and the brainstem volumes and deformations were compared between the AD and the controls. Patients with AD showed significant total volume [(mean ± SD) 21007 ± 1640 mm] reduction in the brainstem compared with the controls [(mean ± SD) 22530 ± 1750 mm] (P<0.001). In addition, AD patients showed significant brainstem deformations in the upper posterior brainstem corresponding to the midbrain compared with the healthy individuals (false discovery rate corrected P<0.05). This study is the first to explore brainstem volume change and deformations in AD. These structural changes in the midbrain areas might be at the core of the underlying neurobiological mechanisms of brainstem dysfunction with relevance to their various cognitive and behavioral symptoms such as memory impairment, sleep, and emotional disturbance in AD. However, further longitudinal studies might be needed to confirm these findings.
由于脑干核与多个皮质结构相互连接，并调节多种自主、认知和行为功能，因此将脑干置于阿尔茨海默病（AD）进展的重要病理核心中可能很重要。尽管已有多项尸检研究报告了AD患者脑干的神经病理学改变，但尚未有对AD患者进行脑干的活体结构神经影像学研究。本研究的目的是调查AD患者与老年正常对照者之间脑干体积和形状的差异。招募了50例AD患者（临床痴呆评定量表≥1）和50例正常对照者，比较了AD组和对照组之间的脑干体积和变形情况。与对照组[（均值±标准差）22530±1750mm³]相比，AD患者的脑干总体积显著减小[（均值±标准差）21007±1640mm³]（P<0.001）。此外，与健康个体相比，AD患者在与中脑相对应的脑干上部后部出现了显著的脑干变形（错误发现率校正P<0.05）。本研究首次探讨了AD患者的脑干体积变化和变形情况。中脑区域的这些结构变化可能是脑干功能障碍潜在神经生物学机制的核心，这与AD患者的各种认知和行为症状有关，如记忆障碍、睡眠和情绪障碍。然而，可能需要进一步的纵向研究来证实这些发现。
