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与神经退行性疾病进展相关的生物膜相关淀粉样蛋白

Biofilm-Associated Amyloid Proteins Linked with the Progression of Neurodegenerative Diseases.

作者信息

Singh Alka Ashok, Khan Fazlurrahman, Song Minseok

机构信息

Department of Life Sciences, Yeungnam University, Gyeongsan 38541, Republic of Korea.

Ocean and Fisheries Development International Cooperation Institute, Pukyong National University, Busan 48513, Republic of Korea.

出版信息

Int J Mol Sci. 2025 Mar 17;26(6):2695. doi: 10.3390/ijms26062695.

Abstract

Biofilm-associated amyloid proteins have emerged as significant contributors to the progression of neurodegenerative diseases, representing a complex intersection of microorganisms and human health. The cross-beta sheet structure characteristic of amyloids produced by gut-colonizing bacteria remains intact, crucial for the resilience of biofilms. These amyloids exacerbate neurodegenerative disorders such as Alzheimer's and Parkinson's by cross-seeding human amyloidogenic proteins like amyloid-beta and α-synuclein, accelerating their misfolding and aggregation. Despite molecular chaperones and heat shock proteins maintaining protein homeostasis, bacterial amyloids can overwhelm them, worsening neuronal damage. Genetic variations in chaperone genes further influence amyloidogenesis and neurodegeneration. Persistent bacterial infections and inflammation compromise the blood-brain barrier, allowing inflammatory molecules and amyloids to enter the brain, perpetuating the cycle of neurodegeneration. The gut-brain axis underscores the impact of dysbiosis and gut microbiota on brain function, potentially contributing to neurodegeneration. The enhancement of biofilm resilience and antibiotic resistance by functional amyloid fibrils complicates the treatment landscape. The interplay among chaperone systems, microbial amyloids, and neurodegenerative diseases underscores the urgent need for advanced treatment strategies targeting these pathways to attenuate disease progression. Understanding the processes that relate biofilm-associated amyloids to the onset of neurological disorders is critical for diagnosing and developing novel treatment strategies.

摘要

生物膜相关的淀粉样蛋白已成为神经退行性疾病进展的重要促成因素,代表了微生物与人类健康的复杂交叉点。肠道定植细菌产生的淀粉样蛋白的交叉β片层结构特征保持完整,这对生物膜的弹性至关重要。这些淀粉样蛋白通过交叉播种人类淀粉样生成蛋白(如β淀粉样蛋白和α-突触核蛋白)加剧阿尔茨海默病和帕金森病等神经退行性疾病,加速它们的错误折叠和聚集。尽管分子伴侣和热休克蛋白维持着蛋白质稳态,但细菌淀粉样蛋白会使其不堪重负,加重神经元损伤。伴侣基因的遗传变异进一步影响淀粉样蛋白生成和神经退行性变。持续性细菌感染和炎症会破坏血脑屏障,使炎症分子和淀粉样蛋白进入大脑,使神经退行性变的循环持续下去。肠-脑轴强调了生态失调和肠道微生物群对脑功能的影响,可能导致神经退行性变。功能性淀粉样纤维增强生物膜弹性和抗生素耐药性,使治疗前景复杂化。伴侣系统、微生物淀粉样蛋白和神经退行性疾病之间的相互作用突出表明,迫切需要针对这些途径的先进治疗策略来减缓疾病进展。了解将生物膜相关淀粉样蛋白与神经系统疾病发作联系起来的过程对于诊断和开发新的治疗策略至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0a2/11942204/b841f6a5ec6d/ijms-26-02695-g002.jpg

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