Torraville Sarah E, Flynn Cassandra M, Kendall Tori L, Yuan Qi
Biomedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, NL A1B 3V6, Canada.
Biomedicines. 2023 Jul 3;11(7):1884. doi: 10.3390/biomedicines11071884.
Alzheimer's disease (AD) is a chronic neurodegenerative disease, characterized by the presence of β-amyloid (Aβ) plaques and neurofibrillary tangles (NFTs) formed from abnormally phosphorylated tau proteins (ptau). To date, there is no cure for AD. Earlier therapeutic efforts have focused on the clinical stages of AD. Despite paramount efforts and costs, pharmaceutical interventions including antibody therapies targeting Aβ have largely failed. This highlights the need to alternate treatment strategies and a shift of focus to early pre-clinical stages. Approximately 25-40% of AD cases can be attributed to environmental factors including chronic stress. Gut dysbiosis has been associated with stress and the pathogenesis of AD and can increase both Aβ and NFTs in animal models of the disease. Both stress and enrichment have been shown to alter AD progression and gut health. Targeting stress-induced gut dysbiosis through probiotic supplementation could provide a promising intervention to delay disease progression. In this review, we discuss the effects of stress, enrichment, and gut dysbiosis in AD models and the promising evidence from probiotic intervention studies.
阿尔茨海默病（AD）是一种慢性神经退行性疾病，其特征是存在由异常磷酸化的tau蛋白（ptau）形成的β-淀粉样蛋白（Aβ）斑块和神经原纤维缠结（NFTs）。迄今为止，尚无治愈AD的方法。早期的治疗努力主要集中在AD的临床阶段。尽管付出了巨大努力和成本，但包括针对Aβ的抗体疗法在内的药物干预大多以失败告终。这凸显了需要改变治疗策略，并将重点转向临床前早期阶段。大约25%-40%的AD病例可归因于包括慢性应激在内的环境因素。肠道微生物群失调与应激及AD的发病机制有关，并且在该疾病的动物模型中会增加Aβ和NFTs。应激和丰富环境都已被证明会改变AD的进展和肠道健康。通过补充益生菌来靶向应激诱导的肠道微生物群失调，可能为延缓疾病进展提供一种有前景的干预措施。在这篇综述中，我们讨论了应激、丰富环境和肠道微生物群失调在AD模型中的作用，以及益生菌干预研究的有前景的证据。
