Impairment of Long-Term Potentiation in Alzheimer's Disease: A computational study based on tripartite synapse structure

机译：阿尔茨海默氏病长期增强的损害：基于三方突触结构的计算研究

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In this work we propose a model to describe impairment of Long-Term Potentiation (LTP) due to Amyloid Beta (Aβ) accumulation during Alzheimer's Disease (AD) in hippocampus. The model embeds astrocyte-neuron interactions and Spike Timing-Dependent Plasticity (STDP) in CA3-CA1 synapses. In our proposed model, considering physiological facts, each astrocyte has a bidirectional signaling with four neurons, consisting of two pre-synaptic and two post-synaptic neurons. Sustained elevation in strength of each synapse leads to an increase in strength of other adjacent synapse, and finally to coupling between those synapses; this is known as LTP. We increased probability of pre-synaptic glutamate release to the level of reported experimental data on AD. As expected, increase of pre-synaptic glutamate release elevates astrocytic calcium. Due to excessive elevation of astrocytic calcium loss of calcium homeostatic, depression in synaptic strength, disruption of slow inward NMDA currents and finally impairment of LTP occur. Our results confirm the hypothesis that although calcium endocytosis is vital to induce LTP, fast and excessive increase of astrocytic calcium makes major problems and impairments for the LTP.

机译：在这项工作中，我们提出了一个模型来描述由于海马阿尔茨海默氏病（AD）期间由于淀粉样β（Aβ）积累而引起的长期增强（LTP）受损。该模型在CA3-CA1突触中嵌入了星形胶质细胞-神经元相互作用和穗定时依赖可塑性（STDP）。在我们提出的模型中，考虑到生理事实，每个星形胶质细胞都有一个包含四个神经元的双向信号，该神经元由两个突触前神经元和两个突触后神经元组成。每个突触强度的持续升高会导致其他相邻突触强度的增加，并最终导致这些突触之间的耦合。这就是所谓的LTP。我们将突触前谷氨酸释放的可能性增加到AD上报道的实验数据的水平。如所预期的，突触前谷氨酸释放的增加提高了星形细胞钙。由于星形胶质细胞钙的过度升高导致稳态钙的损失，突触强度的降低，缓慢的内向NMDA电流的破坏以及最终LTP的损害。我们的结果证实了以下假设：尽管钙内吞作用对于诱导LTP至关重要，但星形细胞钙的快速和过度增加却是LTP的主要问题和损害。

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来源
《2013 20th Iranian Conference on Biomedical Engineering》|2013年|37-41|共5页
会议地点 Tehran(IR)
作者
Roohi Dehkordy Soheila; Bahrami Fariba;
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作者单位

School of ECE, College of Engineering, University of Tehran, Iranc;

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原文格式 PDF
正文语种 eng
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关键词
Alzheimer disease; Long Term Potentiation; beta amyloid; glutamate release probability; tripartite synapse;

机译：阿尔茨海默病；长期增强；β淀粉样蛋白；谷氨酸释放概率；三方突触；;

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1. Pharmacological Rescue of Long-Term Potentiation in Alzheimer Diseased Synapses [J] . Prieto G. Aleph, Trieu Brian H., Dang Cindy T., The Journal of Neuroscience: The Official Journal of the Society for Neuroscience . 2017,第5期

机译：阿尔茨海默氏症患者长期增强的药理拯救
2. The N-methyl-D-aspartate receptor antagonist CPP alters synapse and spine structure and impairs long-term potentiation and long-term depression induced morphological plasticity in dentate gyrus of the awake rat. [J] . Medvedev NI, Popov VI, Rodriguez Arellano J Neuroscience: An International Journal under the Editorial Direction of IBRO . 2010,第4期

机译：N-甲基-D-天冬氨酸受体拮抗剂CPP改变了突触和脊柱的结构，并损害了清醒大鼠齿状回的长期增强和长期抑郁诱导的形态可塑性。
3. Chronic psychosocial stress accelerates impairment of long-term memory and late-phase long-term potentiation in an at-risk model of Alzheimer's disease. [J] . Tran TT, Srivareerat M, Alkadhi KA Hippocampus . 2011,第7期

机译：在阿尔茨海默氏病的高风险模型中，长期的社会心理压力会加速长期记忆和后期长期增强的损害。
4. Impairment of Long-Term Potentiation in Alzheimer's Disease: A computational study based on tripartite synapse structure [C] . Roohi Dehkordy Soheila, Bahrami Fariba Iranian Conference on Biomedical Engineering . 2013

机译：阿尔茨海默病的长期增强障碍：基于三方突触结构的计算研究
5. Studies on the Regulation of Long-term Synapse Stability, Dendrite Maintenance, and Animal Behavior: (1) Laminin-integrin Alpha3 Signaling and (2) Disruption in Alzheimer's Disease Model Mice. [D] . Kerrisk, Meghan Elizabeth. 2014

机译：长期突触稳定性，树突维持和动物行为的调节研究：（1）层粘连蛋白整合素α3信号和（2）阿尔茨海默氏病模型小鼠的破坏。
6. Pharmacological Rescue of Long-Term Potentiation in Alzheimer Diseased Synapses [O] . G. Aleph Prieto, Brian H. Trieu, Cindy T. Dang, 2017

机译：阿尔茨海默氏病突触的长期增强的药理救援
7. The N-methyl-D-aspartate receptor antagonist CPP alters synapse and spine structure and impairs long-term potentiation and long-term depression induced morphological plasticity in dentate gyrus of the awake rat. [O] . Medvedev, Nikolay, Popov, V.I., Rodriguez Arellano, José J., 2010

机译：N-甲基-D-天冬氨酸受体拮抗剂CPP改变了觉醒大鼠齿状回中的突触和脊柱结构，并损害了长期增强和长期抑郁诱导的形态可塑性。

Impairment of Long-Term Potentiation in Alzheimer's Disease: A computational study based on tripartite synapse structure

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