Neuorimaging Laboratory, Santa Lucia Foundation, Rome, Italy.
Hum Brain Mapp. 2013 Dec;34(12):3158-67. doi: 10.1002/hbm.22130. Epub 2012 Jun 19.
A previous preliminary investigation based on a novel MRI approach to map anatomical connectivity revealed areas of increased connectivity in Alzheimer's disease (AD) but not in mild cognitive impairment patients. This prompted the hypothesis tested here, that these areas might reflect phenomena of brain plasticity driven by acetylcholinesterase inhibitors (AChEIs). Thirty-eight patients with probable AD (19 under medication with AChEIs and 19 drug-naïve) were recruited together with 11 healthy controls. All subjects had MRI scanning at 3T, including volumetric and diffusion-weighted scans. Probabilistic tractography was used to initiate streamlines from all parenchymal voxels, and anatomical connectivity maps (ACMs) were obtained by counting, among the total number of streamlines initiated, the fraction passing through each brain voxel. After normalization into standard space, ACMs were used to test for between-group comparisons, and for interactions between the exposure to AChEIs and global level of cognition. Patients with AD had reduced ACM values in the fornix, cingulum, and supramarginal gyri. The ACM value was strongly associated with the AChEI dosage-x-duration product in the anterior limb (non-motor pathway) of the internal capsule. Tractography from this region identified the anterior thalamic radiation as the main white matter (WM) tract passing through it. The reduced connectivity in WM bundles connecting the hippocampi with the rest of the brain (fornix/cingulum) suggests a possible mechanism for the spread of AD pathology. An intriguing explanation for the interaction between AChEIs and ACM is related to the mechanisms of brain plasticity, partially driven by neurotrophic properties of acetylcholine replacement.
先前的一项初步研究基于一种新的 MRI 方法来绘制解剖连接,结果显示阿尔茨海默病(AD)患者的连接增加,但轻度认知障碍患者没有。这促使我们提出了在这里测试的假设,即这些区域可能反映了由乙酰胆碱酯酶抑制剂(AChEIs)驱动的脑可塑性现象。我们招募了 38 名可能患有 AD 的患者(19 名服用 AChEIs,19 名未服用药物),以及 11 名健康对照者。所有受试者均在 3T 磁共振成像扫描仪上进行了 MRI 扫描,包括容积和弥散加权扫描。概率追踪用于从所有实质体素发起流线,通过在发起的总流线数量中计数,获得解剖连通性图谱(ACMs),通过每个脑体素的流线数量。在标准化到标准空间后,使用 ACM 进行组间比较,并进行 AChEI 暴露与整体认知水平之间的交互作用测试。AD 患者的穹窿、扣带和缘上回的 ACM 值降低。ACM 值与内囊前肢(非运动通路)的 AChEI 剂量-持续时间乘积密切相关。该区域的轨迹确定了前丘脑辐射作为主要的通过它的白质(WM)束。连接海马体与大脑其他部位的 WM 束的连接减少(穹窿/扣带)表明 AD 病理学传播的可能机制。AChEI 和 ACM 之间相互作用的一个有趣解释与脑可塑性机制有关,部分机制是由乙酰胆碱替代的神经营养特性驱动的。