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帕金森病痴呆相关基底神经节-皮质并联回路的动态计算模型。

A dynamic computational model of the parallel circuit on the basal ganglia-cortex associated with Parkinson's disease dementia.

机构信息

School of Mathematics and Statistics, Shaanxi Normal University, Xi'an, 710062, People's Republic of China.

出版信息

Biol Cybern. 2024 Apr;118(1-2):127-143. doi: 10.1007/s00422-024-00988-x. Epub 2024 Apr 21.

Abstract

The cognitive impairment will gradually appear over time in Parkinson's patients, which is closely related to the basal ganglia-cortex network. This network contains two parallel circuits mediated by putamen and caudate nucleus, respectively. Based on the biophysical mean-field model, we construct a dynamic computational model of the parallel circuit in the basal ganglia-cortex network associated with Parkinson's disease dementia. The simulated results show that the decrease of power ratio in the prefrontal cortex is mainly caused by dopamine depletion in the caudate nucleus and is less related to that in the putamen, which indicates Parkinson's disease dementia may be caused by a lesion of the caudate nucleus rather than putamen. Furthermore, the underlying dynamic mechanism behind the decrease of power ratio is investigated by bifurcation analysis, which demonstrates that the decrease of power ratio is due to the change of brain discharge pattern from the limit cycle mode to the point attractor mode. More importantly, the spatiotemporal course of dopamine depletion in Parkinson's disease patients is well simulated, which states that with the loss of dopaminergic neurons projecting to the striatum, motor dysfunction of Parkinson's disease is first observed, whereas cognitive impairment occurs after a period of onset of motor dysfunction. These results are helpful to understand the pathogenesis of cognitive impairment and provide insights into the treatment of Parkinson's disease dementia.

摘要

帕金森病患者的认知障碍会随着时间的推移逐渐出现,这与基底节-皮层网络密切相关。该网络包含两个由壳核和尾状核介导的平行回路。基于生物物理平均场模型,我们构建了与帕金森病痴呆相关的基底节-皮层网络中平行回路的动态计算模型。模拟结果表明,前额叶皮层的功率比降低主要是由于尾状核多巴胺耗竭引起的,与壳核多巴胺耗竭关系不大,这表明帕金森病痴呆可能是由尾状核损伤引起的,而不是壳核损伤引起的。此外,通过分岔分析研究了功率比降低的潜在动力学机制,表明功率比降低是由于脑放电模式从极限环模式到点吸引子模式的变化引起的。更重要的是,很好地模拟了帕金森病患者多巴胺耗竭的时空过程,表明随着投射到纹状体的多巴胺能神经元的丧失,首先观察到帕金森病的运动功能障碍,而在运动功能障碍发病一段时间后才出现认知障碍。这些结果有助于了解认知障碍的发病机制,并为帕金森病痴呆的治疗提供了思路。

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