López-Villodres Juan Antonio, Escamilla Alejandro, Mercado-Sáenz Silvia, Alba-Tercedor Carmen, Rodriguez-Perez Luis Manuel, Arranz-Salas Isabel, Sanchez-Varo Raquel, Bermúdez Diego
Departamento Fisiologia Humana, Histologia Humana, Anatomia Patologica y Educacion Fisica y Deportiva, Facultad de Medicina, Universidad de Malaga, 29071 Malaga, Spain.
Instituto de Investigacion Biomedica de Malaga-IBIMA-Plataforma Bionand, 29071 Malaga, Spain.
Biomedicines. 2023 Jun 27;11(7):1846. doi: 10.3390/biomedicines11071846.
In the last decade, the role of the microbiota-gut-brain axis has been gaining momentum in the context of many neurodegenerative and metabolic disorders, including Alzheimer's disease (AD) and diabetes, respectively. Notably, a balanced gut microbiota contributes to the epithelial intestinal barrier maintenance, modulates the host immune system, and releases neurotransmitters and/or neuroprotective short-chain fatty acids. However, dysbiosis may provoke immune dysregulation, impacting neuroinflammation through peripheral-central immune communication. Moreover, lipopolysaccharide or detrimental microbial end-products can cross the blood-brain barrier and induce or at least potentiate the neuropathological progression of AD. Thus, after repeated failure to find a cure for this dementia, a necessary paradigmatic shift towards considering AD as a systemic disorder has occurred. Here, we present an overview of the use of germ-free and/or transgenic animal models as valid tools to unravel the connection between dysbiosis, metabolic diseases, and AD, and to investigate novel therapeutical targets. Given the high impact of dietary habits, not only on the microbiota but also on other well-established AD risk factors such as diabetes or obesity, consistent changes of lifestyle along with microbiome-based therapies should be considered as complementary approaches.
在过去十年中,微生物群-肠-脑轴在许多神经退行性疾病和代谢性疾病(分别包括阿尔茨海默病(AD)和糖尿病)的背景下,其作用日益受到关注。值得注意的是,平衡的肠道微生物群有助于维持肠道上皮屏障、调节宿主免疫系统,并释放神经递质和/或具有神经保护作用的短链脂肪酸。然而,微生物群失调可能引发免疫失调,通过外周-中枢免疫通讯影响神经炎症。此外,脂多糖或有害的微生物终产物可穿过血脑屏障,诱导或至少加剧AD的神经病理进展。因此,在多次未能找到治愈这种痴呆症的方法后,已经发生了一种必要的范式转变,即把AD视为一种全身性疾病。在此,我们概述了使用无菌和/或转基因动物模型作为有效工具,以揭示微生物群失调、代谢性疾病和AD之间的联系,并研究新的治疗靶点。鉴于饮食习惯不仅对微生物群有重大影响,而且对其他已确定的AD风险因素如糖尿病或肥胖也有影响,应将生活方式的持续改变以及基于微生物群的疗法视为补充方法。