用相关神经束造影量化帕金森病6-羟多巴胺模型中局部基底神经节结构连通性的变化。

Mikhail Moshchin, Kevin P Cheng, Susan Osting, Matthew Laluzerne, Samuel A Hurley, Ajay Paul Singh, James K Trevathan, Andrea Brzeczkowski, John-Paul J Yu, Wendell B Lake, Kip A Ludwig, Aaron J Suminski
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摘要

近年来,基于弥散磁共振成像(dMRI)的神经束造影已成为研究帕金森病(PD)等脑部疾病引起的微结构变化的流行工具。定量各向异性(QA)是一种用于确定性纤维跟踪的参数,用于测量大脑区域之间的连接。然而,目前尚不清楚的是,是否可以使用基于离体扩散MRI的束束造影来解决因损伤正中前脑束(MFB)而引起的微结构变化。本研究旨在填补这一空白,为今后PD全脑网络啮齿动物模型结构变化的机制研究奠定基础。具体来说,它评估了相关束造影检测6-羟多巴胺(6-OHDA)损伤大鼠MFB结构变化的能力。研究结果显示,相关纤维束造影可以检测病变MFB的结构变化,并区分6-OHDA组和对照组。影像学结果得到行为学和组织学证据的支持,表明6-OHDA损伤的大鼠确实是帕金森病。结果提示QA和相关神经束造影是检测神经退行性疾病模型局部结构变化的合适方法。更广泛地说,我们期望类似的技术可以提供关于疾病如何改变整个大脑结构的见解,并作为优化治疗干预的工具。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Quantifying changes in local basal ganglia structural connectivity in the 6-hydroxydopamine model of Parkinson's Disease using correlational tractography.

In recent years, tractography based on diffusion magnetic resonance imaging (dMRI) has become a popular tool for studying microstructural changes resulting from brain diseases like Parkinson's Disease (PD). Quantitative anisotropy (QA) is a parameter that is used in deterministic fiber tracking as a measure of connection between brain regions. It remains unclear, however, if microstructural changes caused by lesioning the median forebrain bundle (MFB) to create a Parkinsonian rat model can be resolved using tractography based on ex-vivo diffusion MRI. This study aims to fill this gap and enable future mechanistic research on structural changes of the whole brain network rodent models of PD. Specifically, it evaluated the ability of correlational tractography to detect structural changes in the MFB of 6-hydroxydopamine (6-OHDA) lesioned rats. The findings reveal that correlational tractography can detect structural changes in lesioned MFB and differentiate between the 6-OHDA and control groups. Imaging results are supported by behavioral and histological evidence demonstrating that 6-OHDA lesioned rats were indeed Parkinsonian. The results suggest that QA and correlational tractography is appropriate to examine local structural changes in rodent models of neurodegenerative disease. More broadly, we expect that similar techniques may provide insight on how disease alters structure throughout the brain, and as a tool to optimize therapeutic interventions.

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