Klinik und Poliklinik für Neurologie, Uniklinikum Carl-Gustav Carus, Fetscherstr. 74, 01307, Dresden, Germany.
Neurologische Klinik und Poliklinik, Klinikum der Universität München, Marchioninistr. 15, 81377, Munich, Germany.
Clin Auton Res. 2016 Jun;26(3):211-22. doi: 10.1007/s10286-016-0358-6. Epub 2016 May 13.
Involvement of the peripheral nervous system (PNS) is relatively common in Parkinson's disease (PD) patients. PNS alterations appear early in the course of the disease and are responsible for some of the non-motor symptoms observed in PD patients. In previous studies, we have shown that environmental toxins can trigger the disease by acting on the enteric nervous system.
Here, we analyzed the effect of mitochondrial Complex I inhibition on sympathetic neuritis in vivo and sympathetic neurons in vitro. Combining in vivo imaging and protein expression profiling.
we found that rotenone, a widely used mitochondrial Complex I inhibitor decreases the density of sympathetic neurites innervating the gut in vivo, while in vitro, it induces the redistribution of intracellular alpha-synuclein and neurite degeneration. Interestingly, sympathetic neurons are much more resistant to rotenone exposure than mesencephalic dopaminergic neurons.
Altogether, these results suggest that enteric sympathetic denervation could be an initial pre-motor alteration in PD progression that could be used as an early biomarker of the disease.
帕金森病（PD）患者的周围神经系统（PNS）受累较为常见。PNS 改变在疾病早期出现，并导致 PD 患者出现一些非运动症状。在之前的研究中，我们已经表明，环境毒素可以通过作用于肠神经系统引发疾病。
在这里，我们分析了线粒体复合物 I 抑制剂对体内交感神经神经炎和体外交感神经元的影响。结合体内成像和蛋白质表达谱分析。
我们发现，鱼藤酮，一种广泛使用的线粒体复合物 I 抑制剂，会降低体内支配肠道的交感神经纤维的密度，而在体外，它会诱导细胞内α-突触核蛋白的重新分布和神经突退化。有趣的是，交感神经元对鱼藤酮暴露的抵抗力比中脑多巴胺神经元要强得多。
综上所述，这些结果表明，肠交感神经去神经支配可能是 PD 进展中的一个早期运动前改变，可作为该疾病的早期生物标志物。
