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| 1 | TLR2 and TLR4 in Parkinson’s disease pathogenesis:the environment takes a toll on the gut显示文摘Parkinson's disease(PD)is an incurable,devastating disorder that is characterized by pathological protein aggregation and neurodegeneration in the substantia nigra.In recent years,growing evidence has implicated the gut environment and the gut-brain axis in the pathogenesis and progression of PD,especially in a subset of people who exhibit prodromal gastrointestinal dysfunction.Specifically,perturbations of gut homeostasis are hypothesized to contribute toα-synuclein aggregation in enteric neurons,which may spread to the brain over decades and eventually result in the characteristic central nervous system manifestations of PD,including neurodegeneration and motor impairments.However,the mechanisms linking gut disturbances andα-synuclein aggregation are still unclear.A plethora of research indicates that toll-like receptors(TLRs),especially TLR2 and TLR4;are critical mediators of gut homeostasis.Alongside their established role in innate immunity throughout the body,studies are increasingly demonstrating that TLR2 and TLR4 signalling shapes the development and function of the gut and the enteric nervous system.Notably,TLR2 and TLR4 are dysregulated in patients with PD,and may thus be central to early gut dysfunction in PD.To better understand the putative contribution of intestinal TLR2 and TLR4 dysfunction to earlyα-synuclein aggregation and PD,we critically discuss the role of TLR2 and TLR4 in normal gut function as well as evidence for altered TLR2 and TLR4 signalling in PD;by reviewing clinical,animal model and in vitro research.Growing evidence on the immunological aetiology ofα-synuclein aggregation is also discussed,with a focus on the interactions ofα-synuclein with TLR2 and TLR4.We propose a conceptual model of PD pathogenesis in which microbial dysbiosis alters the permeability of the intestinal barrier as well as TLR2 and TLR4 signalling,ultimately leading to a positive feedback loop of chronic gut dysfunction promotingα-synuclein aggregation in enteric and vagal neurons.In turn,α-synuclein aggregates may then migrate to the brain via peripheral nerves,such as the vagal nerve,to contribute to neuroinflammation and neurodegeneration typically associated with PD. | Anastazja M.Gorecki Chidozie C.Anyaegbu Ryan S.Anderton | 2021 | Translational Neurodegeneration2021，10，4： | 4 |
| 2 | Relationship among Parkinson’s disease, constipation, microbes, and microbiological therapy显示文摘This comprehensive review elucidates the complex interplay between gut microbiota and constipation in Parkinson’s disease(PD),a prevalent non-motor symptom contributing significantly to patients’morbidity.A marked alteration in the gut microbiota,predominantly an increase in the abundance of Proteobacteria and Bacteroidetes,is observed in PD-related constipation.Conventional treatments,although safe,have failed to effectively alleviate symptoms,thereby necessitating the development of novel therapeutic strategies.Microbiological interventions such as prebiotics,probiotics,and fecal microbiota transplantation(FMT)hold therapeutic potential.While prebiotics improve bowel movements,probiotics are effective in enhancing stool consistency and alleviating abdominal discomfort.FMT shows potential for significantly alleviating constipation symptoms by restoring gut microbiota balance in patients with PD.Despite promising developments,the causal relationship between changes in gut microbiota and PD-related constipation remains elusive,highlighting the need for further research in this expanding field. | Xin-Yang Yuan Yu-Sen Chen Zhou Liu | 2024 | World Journal of Gastroenterology2024，30，3： | 0 |
| 3 | 不同月龄A53T小鼠背根神经节中α-Syn表达变化显示文摘目的探讨不同月龄A53T转基因(A53T)小鼠脊髓背根神经节(DRG)中α-突触核蛋白(α-Syn)表达水平的变化。方法6月龄和12月龄野生型(WT)小鼠和A53T小鼠经乌拉坦腹腔麻醉后处死,在体视显微镜下取出胸段、腰段和荐段的DRG组织,采用蛋白免疫印迹法检测DRG中α-Syn的表达水平。结果与相同月龄WT小鼠相比,6月龄及12月龄A53T小鼠DRG中α-Syn表达量显著增加(F=59.164、55.681,P<0.01);与6月龄A53T小鼠相比,12月龄A53T小鼠DRG中α-Syn的表达量显著增加(F=13.802,P<0.05)。结论A53T小鼠DRG中α-Syn表达量高于同月龄WT小鼠,且其表达量随年龄增长而增加。 | 韩帆 焦倩 杜希恂 阎春玲 姜宏 陈曦 | 2023 | 青岛大学学报(医学版)2023，59，3： | 0 |
| 4 | α-syn在不同月龄A53T小鼠小肠中表达变化显示文摘目的探讨不同月龄A53T小鼠小肠组织中α-突触核蛋白(α-syn)表达变化。方法取3月龄和6月龄的野生型(WT)小鼠和A53T小鼠的小肠组织,利用蛋白免疫印迹法和免疫荧光实验检测α-syn的表达水平。结果与同月龄WT组小鼠相比,3月龄、6月龄A53T组小鼠小肠组织α-syn表达量显著增高,差异均有统计学意义(F=3.107、2.955,P<0.05);6月龄A53T组小鼠小肠组织α-syn表达量比3月龄A53T组小鼠增加21.71%,两组相比差异具有显著性(F=2.836,P<0.05)。免疫荧光实验显示,与同月龄WT组小鼠相比,A53T组小鼠小肠组织α-syn表达量显著增高;6月龄A53T组小鼠小肠组织α-syn表达量明显高于3月龄A53T组。结论A53T小鼠小肠组织α-syn表达量高于同月龄WT小鼠,且其小肠组织α-syn表达量随年龄增长而增加。 | 刘玫秋 陈曦 姜宏 | 2022 | 青岛大学学报(医学版)2022，58，3： | 0 |
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