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扩散峰度成像检测到甲基苯丙胺诱导的帕金森病小鼠模型中的微观结构变化。

Diffusion Kurtosis Imaging Detects Microstructural Changes in a Methamphetamine-Induced Mouse Model of Parkinson's Disease.

机构信息

Department of Pharmacology, Faculty of Medicine, Masaryk University, Kamenice 5, 625 00, Brno, Czech Republic.

Applied Neuroscience Research Group, CEITEC - Central European Institute of Technology, Masaryk University, Brno, Czech Republic.

出版信息

Neurotox Res. 2019 Nov;36(4):724-735. doi: 10.1007/s12640-019-00068-0. Epub 2019 Jun 18.

Abstract

Methamphetamine (METH) abuse is known to increase the risk of Parkinson's disease (PD) due to its dopaminergic neurotoxicity. This is the rationale for the METH model of PD developed by toxic METH dosing (10 mg/kg four times every 2 h) which features robust neurodegeneration and typical motor impairment in mice. In this study, we used diffusion kurtosis imaging to reveal microstructural brain changes caused by METH-induced neurodegeneration. The METH-treated mice and saline-treated controls underwent diffusion kurtosis imaging scanning using the Bruker Avance 9.4 Tesla MRI system at two time-points: 5 days and 1 month to capture both early and late changes induced by METH. At 5 days, we found a decrease in kurtosis in substantia nigra, striatum and sensorimotor cortex, which is likely to indicate loss of DAergic neurons. At 1 month, we found an increase of kurtosis in striatum and sensorimotor cortex and hippocampus, which may reflect certain recovery processes. Furthermore, we performed tract-based spatial statistics analysis in the white matter and at 1 month, we observed increased kurtosis in ventral nucleus of the lateral lemniscus and some of the lateral thalamic nuclei. No changes were present at the early stage. This study confirms the ability of diffusion kurtosis imaging to detect microstructural pathological processes in both grey and white matter in the METH model of PD. The exact mechanisms underlying the kurtosis changes remain to be elucidated but kurtosis seems to be a valuable biomarker for tracking microstructural brain changes in PD and potentially other neurodegenerative disorders.

摘要

甲基苯丙胺(METH)滥用会因其多巴胺能神经毒性而增加帕金森病(PD)的风险。这就是通过有毒 METH 剂量(10mg/kg,每 2 小时 4 次)开发 PD 的 METH 模型的原理,该模型在小鼠中具有强大的神经退行性变和典型的运动障碍。在这项研究中,我们使用扩散峰度成像来揭示由 METH 诱导的神经退行性变引起的大脑微观结构变化。METH 处理的小鼠和盐水处理的对照小鼠在两个时间点(5 天和 1 个月)使用 Bruker Avance 9.4T MRI 系统进行扩散峰度成像扫描,以捕捉 METH 诱导的早期和晚期变化。在 5 天时,我们发现黑质、纹状体和感觉运动皮层的峰度降低,这可能表明 DA 能神经元丢失。在 1 个月时,我们发现纹状体和感觉运动皮层以及海马体的峰度增加,这可能反映了某些恢复过程。此外,我们在白质中进行了基于束的空间统计学分析,在 1 个月时,我们观察到外侧丘系腹核和一些外侧丘脑核的峰度增加。在早期没有变化。这项研究证实了扩散峰度成像能够检测 PD 的 METH 模型中灰质和白质微观结构病理过程的能力。峰度变化的确切机制仍有待阐明,但峰度似乎是跟踪 PD 和潜在其他神经退行性疾病中大脑微观结构变化的有价值的生物标志物。

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