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红核在帕金森病补偿中的作用可能解释了为什么灵长类动物可以患上稳定的帕金森病。

Involvement of the Red Nucleus in the Compensation of Parkinsonism may Explain why Primates can develop Stable Parkinson's Disease.

机构信息

Animal Science Department, Biomedical Primate Research Centre (BPRC), P.O. Box 3306, 2280 GH, Rijswijk, The Netherlands.

Department of Immunobiology, Biomedical Primate Research Centre (BPRC), P.O. Box 3306, 2280 GH, Rijswijk, The Netherlands.

出版信息

Sci Rep. 2019 Jan 29;9(1):880. doi: 10.1038/s41598-018-37381-1.

DOI:10.1038/s41598-018-37381-1
PMID:30696912
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6351580/
Abstract

Neurological compensatory mechanisms help our brain to adjust to neurodegeneration as in Parkinson's disease. It is suggested that the compensation of the damaged striato-thalamo-cortical circuit is focused on the intact thalamo-rubro-cerebellar pathway as seen during presymptomatic Parkinson, paradoxical movement and sensorimotor rhythm (SMR). Indeed, the size of the red nucleus, connecting the cerebellum with the cerebral cortex, is larger in Parkinson's disease patients suggesting an increased activation of this brain area. Therefore, the red nucleus was examined in MPTP-induced parkinsonian marmoset monkeys during the presymptomatic stage and after SMR activation by neurofeedback training. We found a reverse significant correlation between the early expression of parkinsonian signs and the size of the parvocellular part of the red nucleus, which is predominantly present in human and non-human primates. In quadrupedal animals it consists mainly of the magnocellular part. Furthermore, SMR activation, that mitigated parkinsonian signs, further increased the size of the red nucleus in the marmoset monkey. This plasticity of the brain helps to compensate for dysfunctional movement control and can be a promising target for compensatory treatment with neurofeedback technology, vibrotactile stimulation or DBS in order to improve the quality of life for Parkinson's disease patients.

摘要

神经补偿机制有助于大脑适应神经退行性疾病,如帕金森病。有研究表明,在帕金森病前期、反常运动和感觉运动节律(SMR)中,受损纹状体-丘脑-皮质回路的补偿集中在完整的丘脑-红核-小脑通路。事实上,连接小脑和大脑皮层的红核体积在帕金森病患者中更大,这表明该脑区的激活增加。因此,我们在 MPTP 诱导的帕金森病恒河猴的前期阶段和 SMR 通过神经反馈训练激活后,检查了红核。我们发现,帕金森病早期症状的表达与红核的小细胞部分大小呈显著负相关,而小细胞部分主要存在于人类和非人类灵长类动物中。在四足动物中,它主要由大细胞部分组成。此外,减轻帕金森病症状的 SMR 激活进一步增加了恒河猴红核的大小。这种大脑的可塑性有助于补偿运动控制的功能障碍,并且可以成为使用神经反馈技术、振动刺激或 DBS 进行补偿性治疗的有前途的目标,以提高帕金森病患者的生活质量。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7d7/6351580/8ffb4736dc51/41598_2018_37381_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7d7/6351580/03ce57863d91/41598_2018_37381_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7d7/6351580/54bf3989548b/41598_2018_37381_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7d7/6351580/8ffb4736dc51/41598_2018_37381_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7d7/6351580/03ce57863d91/41598_2018_37381_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7d7/6351580/54bf3989548b/41598_2018_37381_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7d7/6351580/8ffb4736dc51/41598_2018_37381_Fig3_HTML.jpg

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