Mahbub Nasir Uddin, Islam Md Minarul, Hong Seong-Tshool, Chung Hea-Jong
Department of Biomedical Sciences and Institute for Medical Science, Jeonbuk National University Medical School, Jeonju, Republic of Korea.
Gwangju Center, Korea Basic Science Institute, Gwangju, Republic of Korea.
Front Cell Infect Microbiol. 2024 Feb 16;14:1348279. doi: 10.3389/fcimb.2024.1348279. eCollection 2024.
Abnormal behavior of α-synuclein and prion proteins is the hallmark of Parkinson's disease (PD) and prion illnesses, respectively, being complex neurological disorders. A primary cause of protein aggregation, brain injury, and cognitive loss in prion illnesses is the misfolding of normal cellular prion proteins (PrP) into an infectious form (PrP). Aggregation of α-synuclein causes disruptions in cellular processes in Parkinson's disease (PD), leading to loss of dopamine-producing neurons and motor symptoms. Alteration in the composition or activity of gut microbes may weaken the intestinal barrier and make it possible for prions to go from the gut to the brain. The gut-brain axis is linked to neuroinflammation; the metabolites produced by the gut microbiota affect the aggregation of α-synuclein, regulate inflammation and immunological responses, and may influence the course of the disease and neurotoxicity of proteins, even if their primary targets are distinct proteins. This thorough analysis explores the complex interactions that exist between the gut microbiota and neurodegenerative illnesses, particularly Parkinson's disease (PD) and prion disorders. The involvement of the gut microbiota, a complex collection of bacteria, archaea, fungi, viruses etc., in various neurological illnesses is becoming increasingly recognized. The gut microbiome influences neuroinflammation, neurotransmitter synthesis, mitochondrial function, and intestinal barrier integrity through the gut-brain axis, which contributes to the development and progression of disease. The review delves into the molecular mechanisms that underlie these relationships, emphasizing the effects of microbial metabolites such as bacterial lipopolysaccharides (LPS), and short-chain fatty acids (SCFAs) in regulating brain functioning. Additionally, it looks at how environmental influences and dietary decisions affect the gut microbiome and whether they could be risk factors for neurodegenerative illnesses. This study concludes by highlighting the critical role that the gut microbiota plays in the development of Parkinson's disease (PD) and prion disease. It also provides a promising direction for future research and possible treatment approaches. People afflicted by these difficult ailments may find hope in new preventive and therapeutic approaches if the role of the gut microbiota in these diseases is better understood.
α-突触核蛋白和朊病毒蛋白的异常行为分别是帕金森病（PD）和朊病毒病的标志，这两种都是复杂的神经疾病。朊病毒病中蛋白质聚集、脑损伤和认知丧失的主要原因是正常细胞朊病毒蛋白（PrP）错误折叠成感染性形式（PrP）。α-突触核蛋白的聚集导致帕金森病（PD）细胞过程中断，导致产生多巴胺的神经元丧失和运动症状。肠道微生物组成或活性的改变可能会削弱肠道屏障，使朊病毒从肠道进入大脑成为可能。肠-脑轴与神经炎症有关；肠道微生物群产生的代谢物会影响α-突触核蛋白的聚集，调节炎症和免疫反应，甚至可能影响疾病进程和蛋白质的神经毒性，即使它们的主要靶点是不同的蛋白质。这项深入分析探讨了肠道微生物群与神经退行性疾病，特别是帕金森病（PD）和朊病毒疾病之间存在的复杂相互作用。肠道微生物群是细菌、古细菌、真菌、病毒等的复杂集合，其在各种神经疾病中的作用越来越受到认可。肠道微生物组通过肠-脑轴影响神经炎症、神经递质合成、线粒体功能和肠道屏障完整性，这有助于疾病的发展和进展。该综述深入研究了这些关系背后的分子机制，强调了微生物代谢物如细菌脂多糖（LPS）和短链脂肪酸（SCFAs）在调节大脑功能方面的作用。此外，它还研究了环境影响和饮食选择如何影响肠道微生物组，以及它们是否可能是神经退行性疾病的风险因素。本研究最后强调了肠道微生物群在帕金森病（PD）和朊病毒病发展中所起的关键作用。它还为未来的研究和可能的治疗方法提供了一个有前景的方向。如果能更好地理解肠道微生物群在这些疾病中的作用，那么受这些疑难病症折磨的人们可能会在新的预防和治疗方法中找到希望。
