突触核蛋白与多巴胺：帕金森病的“邦妮与克莱德”。 - Suppr | 超能文献

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Synuclein and dopamine: the Bonnie and Clyde of Parkinson's disease.突触核蛋白与多巴胺：帕金森病的“邦妮与克莱德”。

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Age-dependent nigral dopaminergic neurodegeneration and α-synuclein accumulation in RGS6-deficient mice.RGS6 缺陷型小鼠的年龄依赖性黑质多巴胺能神经退行性变和α-突触核蛋白积累。

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A tango for two: Dopamine and α-synuclein synergy may explain nigrostriatal degeneration in Parkinson's disease.双人探戈：多巴胺与α-突触核蛋白的协同作用或许能解释帕金森病中的黑质纹状体变性。

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Mutant α-Synuclein Overexpression Induces Stressless Pacemaking in Vagal Motoneurons at Risk in Parkinson's Disease.突变型α-突触核蛋白过表达在帕金森病高危迷走运动神经元中诱导无应激性起搏。

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Could a loss of alpha-synuclein function put dopaminergic neurons at risk?α-突触核蛋白功能丧失会使多巴胺能神经元处于危险之中吗？

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Parkinson-like neurodegeneration induced by targeted overexpression of alpha-synuclein in the nigrostriatal system.黑质纹状体系统中α-突触核蛋白靶向过表达诱导的帕金森样神经退行性变。

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Alpha-synuclein in colonic submucosa in early untreated Parkinson's disease.早期未经治疗的帕金森病患者结肠黏膜下层的α-突触核蛋白。

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Iron, Dopamine, and α-Synuclein Interactions in at-Risk Dopaminergic Neurons in Parkinson's Disease.帕金森病中高危多巴胺能神经元内铁、多巴胺与α-突触核蛋白的相互作用

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Overexpression of alpha-synuclein in rat substantia nigra results in loss of dopaminergic neurons, phosphorylation of alpha-synuclein and activation of caspase-9: resemblance to pathogenetic changes in Parkinson's disease.大鼠黑质中α-突触核蛋白的过表达导致多巴胺能神经元丧失、α-突触核蛋白磷酸化及半胱天冬酶-9激活：类似于帕金森病的致病变化。

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Chitosan alleviates symptoms of Parkinson's disease by reducing acetate levels, which decreases inflammation and promotes repair of the intestinal barrier and blood-brain barrier.壳聚糖通过降低醋酸盐水平来缓解帕金森病症状，这会减少炎症并促进肠屏障和血脑屏障的修复。

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Molecular crosstalk between circadian clock and NLRP3 inflammasome signaling in Parkinson's disease.帕金森病中昼夜节律与NLRP3炎性小体信号通路之间的分子串扰

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本文引用的文献

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Dopamine induces soluble α-synuclein oligomers and nigrostriatal degeneration.多巴胺诱导可溶性α-突触核蛋白寡聚体和黑质纹状体变性。

Nat Neurosci. 2017 Nov;20(11):1560-1568. doi: 10.1038/nn.4641. Epub 2017 Sep 18.

2

Synucleins Have Multiple Effects on Presynaptic Architecture.突触核蛋白对突触前结构有多种影响。

Cell Rep. 2017 Jan 3;18(1):161-173. doi: 10.1016/j.celrep.2016.12.023.

3

Acute increase of α-synuclein inhibits synaptic vesicle recycling evoked during intense stimulation.α-突触核蛋白的急性增加会抑制强烈刺激期间诱发的突触小泡循环。