Rout Monalisa, Prusty Shakti Ketan, Kar Durga Madhab
School of Pharmaceutical Sciences, Siksha O Anusandhan deemed to be University, Bhubaneswar, India.
Curr Rev Clin Exp Pharmacol. 2024 Dec 23. doi: 10.2174/0127724328332572241219102122.
The estimated worldwide number of individuals diagnosed with Parkinson's disease (PD) might exceed 10 million by 2040. However, the underlying evidence for PD is unclear. Recent research in Parkinson's disease has focused on exploring the gut-brain axis. Researchers have proposed that gut microbiota and gut dysbiosis contribute to peripheral inflammatory conditions. The involvement of gut pathogens and dysbiosis in peripheral inflammatory diseases has been hypothesized. In Parkinson's disease, the metabolic effects associated with gut dysbiosis accelerate nerve cell loss and damage. The microbiota-gut-brain axis (MGBA) establishes the relationship between the brain and the gut through the bidirectional vagus nerve. The MGBA promotes digestive system regulation and is responsible for maintaining metabolic homeostasis under regular conditions. Helicobacter pylori, Enterococcus faecalis, and Desulfovibrio are gut bacteria whose relative abundance has been associated with Parkinson's disease etiology and treatment efficacy. Numerous clinical and preclinical studies have substantiated the therapeutic potential of probiotics in treating Parkinson's disease via the gut-brain axis. The technique appears to have benefited from a combination of favorable conditions that led to its success. The present study investigated whether administering the probiotic can be a better therapeutic intervention for PD or not. Although widespread, no medicines exist to halt the neurodegenerative effects of PD. Some probiotics raised brain dopamine levels, slowed or stopped neuronal death, and improved motor function in models of toxin-induced and genetic PD in mice, rats, flies, and induced pluripotent stem cells. Probiotics control gut dysbiosis, thereby preventing neurodegeneration in PD via the gut-brain axis. Probiotics are used to control the principal dangers of oxidative stress and alpha-synuclein (α-synuclein) aggregation. Probiotics, which contain beneficial microorganisms such as Lactobacillus, Blautia, Roseburia, Lachnospiraceae, Prevotellaceae, and Akkermansia, may help alleviate PD symptoms and slow the disease's progression. Numerous probiotic bacteria can treat the neurodegenerative condition. As a result, this review paper focuses on the current understanding of the link between PD and gut microbiota while also providing comprehensive information about the neuroprotective function of probiotics.
到2040年，全球帕金森病（PD）确诊患者估计数量可能超过1000万。然而，PD的潜在病因尚不清楚。帕金森病的最新研究集中在探索肠-脑轴。研究人员提出，肠道微生物群和肠道生态失调会导致外周炎症状态。肠道病原体和生态失调与外周炎症性疾病的关联已被提出假设。在帕金森病中，与肠道生态失调相关的代谢效应会加速神经细胞的损失和损伤。微生物群-肠-脑轴（MGBA）通过双向迷走神经建立大脑与肠道之间的关系。MGBA促进消化系统调节，并在正常情况下负责维持代谢稳态。幽门螺杆菌、粪肠球菌和脱硫弧菌是肠道细菌，它们的相对丰度与帕金森病的病因和治疗效果有关。大量临床和临床前研究证实了益生菌通过肠-脑轴治疗帕金森病的潜在疗效。该技术似乎受益于多种有利条件的结合，从而取得了成功。本研究调查了给予益生菌是否能成为治疗PD的更好的治疗干预措施。尽管PD很常见，但目前尚无药物能够阻止其神经退行性作用。一些益生菌可提高大脑多巴胺水平，减缓或阻止神经元死亡，并改善小鼠（模型）、大鼠、果蝇和诱导多能干细胞中毒素诱导和遗传性帕金森病模型的运动功能。益生菌可控制肠道生态失调，从而通过肠-脑轴预防帕金森病中的神经退行性变。益生菌用于控制氧化应激和α-突触核蛋白（α-synuclein）聚集的主要风险。含有有益微生物（如乳酸杆菌、布劳特氏菌、罗斯伯里氏菌、毛螺菌科、普雷沃氏菌科和阿克曼氏菌）的益生菌可能有助于缓解帕金森病症状并减缓疾病进展。许多益生菌可治疗这种神经退行性疾病。因此，本综述文章重点关注了目前对帕金森病与肠道微生物群之间联系的理解，同时也提供了有关益生菌神经保护功能的全面信息。
