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探索粪菌移植调节帕金森病炎症的作用:炎症标志物及潜在影响的综述。

Exploring Fecal Microbiota Transplantation for Modulating Inflammation in Parkinson's Disease: A Review of Inflammatory Markers and Potential Effects.

机构信息

Students Scientific Group NEKON by the Department of Neurology, Faculty of Health Science, Medical University of Warsaw, 03-242 Warsaw, Poland.

Department of Neurology, Faculty of Health Science, Medical University of Warsaw, 03-242 Warsaw, Poland.

出版信息

Int J Mol Sci. 2024 Jul 15;25(14):7741. doi: 10.3390/ijms25147741.

Abstract

Parkinson's disease (PD) is a complex neurodegenerative disorder characterized by numerous motor and non-motor symptoms. Recent data highlight a potential interplay between the gut microbiota and the pathophysiology of PD. The degeneration of dopaminergic neurons in PD leads to motor symptoms (tremor, rigidity, and bradykinesia), with antecedent gastrointestinal manifestations, most notably constipation. Consequently, the gut emerges as a plausible modulator in the neurodegenerative progression of PD. Key molecular changes in PD are discussed in the context of the gut-brain axis. Evidence suggests that the alterations in the gut microbiota composition may contribute to gastroenteric inflammation and influence PD symptoms. Disturbances in the levels of inflammatory markers, including tumor necrosis factor-α (TNF α), interleukin -1β (IL-1β), and interleukin-6 (IL-6), have been observed in PD patients. These implicate the involvement of systemic inflammation in disease pathology. Fecal microbiota transplantation emerges as a potential therapeutic strategy for PD. It may mitigate inflammation by restoring gut homeostasis. Preclinical studies in animal models and initial clinical trials have shown promising results. Overall, understanding the interplay between inflammation, the gut microbiota, and PD pathology provides valuable insights into potential therapeutic interventions. This review presents recent data about the bidirectional communication between the gut microbiome and the brain in PD, specifically focusing on the involvement of inflammatory biomarkers.

摘要

帕金森病(PD)是一种复杂的神经退行性疾病,其特征是存在多种运动和非运动症状。最近的数据强调了肠道微生物群与 PD 病理生理学之间存在潜在的相互作用。PD 中多巴胺能神经元的退化导致运动症状(震颤、僵硬和运动迟缓),其前驱胃肠道表现最明显的是便秘。因此,肠道成为 PD 神经退行性进展中一个合理的调节剂。在肠道-大脑轴的背景下讨论了 PD 中的关键分子变化。有证据表明,肠道微生物群组成的改变可能导致胃肠道炎症,并影响 PD 症状。PD 患者观察到炎症标志物(包括肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6))水平的紊乱。这表明全身炎症参与了疾病病理。粪便微生物群移植作为 PD 的一种潜在治疗策略出现。它可以通过恢复肠道内稳态来减轻炎症。动物模型的临床前研究和初步临床试验显示出有希望的结果。总的来说,了解炎症、肠道微生物群和 PD 病理学之间的相互作用为潜在的治疗干预提供了有价值的见解。这篇综述介绍了关于 PD 中肠道微生物组和大脑之间双向通讯的最新数据,特别关注炎症生物标志物的参与。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4882/11277532/7e3f58e32256/ijms-25-07741-g001.jpg

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