Siripaopradit Yada, Chatsirisakul Oranut, Ariyapaisalkul Tassanee, Sereemaspun Amornpun
Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Center of Excellence in Nanomedicine, Department of Anatomy, Faculty of Medicine, Chulalongkorn University, 1873 Rama 4 Road, Pathumwan, Bangkok, 10330, Thailand.
BMC Neurol. 2024 Dec 19;24(1):481. doi: 10.1186/s12883-024-03978-5.
Alzheimer's disease (AD) is a prevalent neurodegenerative disorder in the elderly, causing cognitive impairment. Its pathogenesis is characterized by amyloid beta deposition, neurofibrillary tangles, and neuroinflammation. Recent research has identified the link between gut dysbiosis, an imbalance of intestinal microorganisms, to this pathogenesis via the gut-brain axis. This study aims to review the probiotics' therapeutic effect, targeting the gut-brain axis, for AD treatment in animals.
The method utilized in this study followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guideline. Three reviewers searched articles through PubMed, Scopus, and Embase using advanced search strategy. Articles published between 2010 and 2023 that met the criteria were included.
Of 2,273 articles, 21 animal studies measuring the effects of probiotics genera Lactobacillus and/or Bifidobacterium on AD via at least one of these four outcomes: AD pathology, cognitive function, neuroinflammation, and gut microbiota composition. The results demonstrated that probiotics could repair gut dysbiosis by decreasing pro-inflammatory bacteria and increasing anti-inflammatory bacteria. Repaired dysbiosis was found to be associated with less neuroinflammation as significant reductions in neuroinflammatory markers related to the pathogenesis of AD such as TNF-α (SMD = -2.08, P = 0.005), IL-6 (SMD = -2.98, P < 0.0005), and IL-1β (SMD = -2.49, P = 0.003) were observed. Reduced amyloid beta deposition (SMD = -1.17, P = 0.009) was reported, but reduction in tau hyperphosphorylation was found to be insignificant. For cognitive function, positive results were demonstrated for all three aspects of cognitive function including long-term memory (SMD = 2.55, P < 0.00001), short-term memory (SMD = 1.32, P = 0.003), and spatial recognition (SMD = -1.13, P < 0.00001).
Particular formulas of probiotics showed potential effectiveness in AD therapies with demonstrated association with the gut-brain axis. Future studies are required to investigate strain-specific results and optimal dosages and regimens.
阿尔茨海默病(AD)是老年人中一种常见的神经退行性疾病,会导致认知障碍。其发病机制的特征是β-淀粉样蛋白沉积、神经原纤维缠结和神经炎症。最近的研究通过肠-脑轴确定了肠道微生物群失衡(肠道微生物失调)与这种发病机制之间的联系。本研究旨在综述益生菌针对肠-脑轴在动物AD治疗中的治疗效果。
本研究采用的方法遵循系统评价和Meta分析的首选报告项目(PRISMA)指南。三位评审员使用高级搜索策略在PubMed、Scopus和Embase上搜索文章。纳入了2010年至2023年发表的符合标准的文章。
在2273篇文章中,有21项动物研究通过以下四个结果中的至少一项来衡量益生菌属乳酸杆菌和/或双歧杆菌对AD的影响:AD病理学、认知功能、神经炎症和肠道微生物群组成。结果表明,益生菌可以通过减少促炎细菌和增加抗炎细菌来修复肠道微生物失调。发现修复后的失调与较少的神经炎症有关,因为与AD发病机制相关的神经炎症标志物如TNF-α(标准化均数差[SMD]= -2.08,P = 0.005)、IL-6(SMD = -2.98,P < 0.0005)和IL-1β(SMD = -2.49,P = 0.003)显著降低。报告了β-淀粉样蛋白沉积减少(SMD = -1.17,P = 0.009),但发现tau蛋白过度磷酸化的减少不显著。对于认知功能,在认知功能的所有三个方面都显示出积极结果,包括长期记忆(SMD = 2.55,P < 0.00001)、短期记忆(SMD = 1.32,P = 0.003)和空间识别(SMD = -1.13,P < 0.00001)。
特定配方的益生菌在AD治疗中显示出潜在疗效,且与肠-脑轴存在关联。未来需要研究特定菌株的结果以及最佳剂量和方案。