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神经调节在体内改变α-突触核蛋白的传播动力学,且这种模式可通过全脑功能的变化来预测。

Neuromodulation modifies α-synuclein spreading dynamics in vivo and the pattern is predicted by changes in whole-brain function.

作者信息

Dadgar-Kiani Ehsan, Bieri Gregor, Melki Ronald, Hossain Aronee, Gitler Aaron D, Lee Jin Hyung

机构信息

Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA, 94305, USA; Department of Bioengineering, Stanford University, Stanford, CA, 94305, USA.

Department of Genetics, Stanford University, CA, 94305, USA.

出版信息

Brain Stimul. 2024 Jul-Aug;17(4):938-946. doi: 10.1016/j.brs.2024.07.021. Epub 2024 Aug 2.

Abstract

BACKGROUND

Many neurodegenerative disease treatments, such as deep brain stimulation for Parkinson's Disease, can alleviate symptoms by primarily compensating for circuit dysfunctions. However, the stimulation's effect on the underlying disease progression remains relatively unknown. Here, we report that neuromodulation can not only modulate circuit function but also modulate the in vivo spreading dynamics of α-synuclein pathology, the primary pathological hallmark observed in Parkinson's Disease.

METHODS

In a mouse model, pre-formed fibrils were injected into the striatum to induce widespread α-synuclein pathology. Two days after fibril injection, mice were treated for two weeks with daily optogenetic stimulation of the Secondary Motor Area, Layer V. Whole brains were then extracted, immunolabeled, cleared, and imaged with light-sheet fluorescent microscopy.

RESULTS

Repeated optogenetic stimulation led to a decrease in pathology at the site of stimulation and at various cortical and subcortical regions, while the contralateral cortex saw a consistent increase. Aligning the pathology changes with optogenetic-fMRI measured brain activity, we found that the changes in pathology and brain function had similar spatial locations but opposite polarity.

CONCLUSION

These results demonstrate the ability to modulate and predict whole brain pathology changes using neuromodulation, opening a new horizon for investigating optimized neuromodulation therapies.

摘要

背景

许多神经退行性疾病的治疗方法,如用于帕金森病的深部脑刺激,主要通过补偿神经回路功能障碍来缓解症状。然而,刺激对潜在疾病进展的影响仍相对未知。在此,我们报告神经调节不仅可以调节神经回路功能,还可以调节α-突触核蛋白病变在体内的传播动态,α-突触核蛋白病变是帕金森病中观察到的主要病理特征。

方法

在一个小鼠模型中,将预先形成的纤维注射到纹状体中以诱导广泛的α-突触核蛋白病变。在纤维注射两天后,对小鼠进行为期两周的每日光遗传学刺激,刺激部位为二级运动区第五层。然后取出整个大脑,进行免疫标记、清除,并用光片荧光显微镜成像。

结果

重复的光遗传学刺激导致刺激部位以及各个皮质和皮质下区域的病变减少,而对侧皮质则持续增加。将病变变化与光遗传学功能磁共振成像测量的脑活动进行比对,我们发现病变和脑功能的变化具有相似的空间位置但极性相反。

结论

这些结果证明了利用神经调节来调节和预测全脑病变变化的能力,为研究优化的神经调节疗法开辟了新的视野。

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