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益生菌、益生元及后生元的作用:阿尔茨海默病中胶质细胞激活的细胞及分子途径

The role of probiotics, prebiotics, and postbiotics: cellular and molecular pathways activated on glial cells in Alzheimer's disease.

作者信息

Patricio-Martínez Aleidy, Patricio Felipe, Macuil-Chapuli Edgar, Martínez-Juárez Enoc Álvaro, Flores-Díaz Steven, Cedillo-Ramírez María Lilia, Limón Ilhuicamina Daniel

机构信息

Laboratorio de Neurofarmacología-Facultad de Ciencias Químicas-Benemérita Universidad Autónoma de Puebla, Puebla, Mexico.

Facultad de Ciencias Biológicas-Benemérita Universidad Autónoma de Puebla, Puebla, Mexico.

出版信息

Front Neurosci. 2025 Jun 25;19:1598011. doi: 10.3389/fnins.2025.1598011. eCollection 2025.

Abstract

Supplementation with prebiotics and probiotics can modulate the intestinal microbiota, returning it to a more physiological state; therefore, they can be considered as a possible treatment in many prevalent conditions, including neurodegenerative diseases. Alzheimer's disease (AD) is the most common form of dementia, accounting for 60 to 70% of cases. The neuropathological features of AD include neuritic plaques (extracellular deposits of the beta-amyloid protein, Aβ), neurofibrillary tangles (resulting from hyperphosphorylation of the tau protein), a predominantly cholinergic synaptic decrease, and the presence of inflammatory markers, all these characteristics together trigger the neurodegenerative process and cognitive deterioration. The etiology of AD is multifactorial, however, in recent years evidence has been shown on the significant association between dysbiosis, neuroinflammation, and neurodegeneration. In the present review, we will discuss the role of gut microbiota in the pathogenesis of AD, as well as the underlying mechanisms that trigger the use of probiotics, prebiotics, and postbiotics in neuroinflammation. Our attention will focus on the cellular and molecular mechanisms triggered by astrocytes and microglia, cells involved in mediating neuroinflammation and neurodegeneration in AD.

摘要

补充益生元和益生菌可以调节肠道微生物群,使其恢复到更接近生理状态;因此,在包括神经退行性疾病在内的许多常见病症中,它们可被视为一种可能的治疗方法。阿尔茨海默病(AD)是最常见的痴呆形式,占病例的60%至70%。AD的神经病理学特征包括神经炎性斑块(β-淀粉样蛋白Aβ的细胞外沉积物)、神经原纤维缠结(由tau蛋白的过度磷酸化导致)、主要的胆碱能突触减少以及炎症标志物的存在,所有这些特征共同引发神经退行性过程和认知衰退。AD的病因是多因素的,然而,近年来已有证据表明肠道微生物群失调、神经炎症和神经退行性变之间存在显著关联。在本综述中,我们将讨论肠道微生物群在AD发病机制中的作用,以及在神经炎症中触发使用益生菌、益生元和后生元的潜在机制。我们将重点关注星形胶质细胞和小胶质细胞触发的细胞和分子机制,这些细胞参与介导AD中的神经炎症和神经退行性变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34f2/12237913/21a397f15cfa/fnins-19-1598011-g001.jpg

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