阿尔茨海默病的肠道微生物群-宿主脂质串扰：对疾病进展和治疗的影响

IF 14.9 1区医学 Q1 NEUROSCIENCES

Molecular Neurodegeneration Pub Date : 2024-04-16 DOI:10.1186/s13024-024-00720-0

Ya-Xi Luo, Ling-Ling Yang, Xiu-Qing Yao

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引用次数: 0

摘要

人体内数以万亿计的肠道细菌会随着生理和病理变化而发生动态变化。它们的组成和代谢物的改变共同导致了阿尔茨海默病的进展。肠道微生物群在阿尔茨海默病中的作用是多样而复杂的，有证据表明脂质代谢可能是潜在的途径之一。然而，肠道微生物群在阿尔茨海默病病理过程中介导脂质代谢的机制仍不清楚，需要进一步研究才能明确。本综述重点介绍目前对肠道微生物群如何扰乱脂质代谢的理解，并根据现有数据讨论这些发现在指导阿尔茨海默病预防或治疗策略方面的意义。

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Gut microbiota-host lipid crosstalk in Alzheimer’s disease: implications for disease progression and therapeutics

Trillions of intestinal bacteria in the human body undergo dynamic transformations in response to physiological and pathological changes. Alterations in their composition and metabolites collectively contribute to the progression of Alzheimer’s disease. The role of gut microbiota in Alzheimer’s disease is diverse and complex, evidence suggests lipid metabolism may be one of the potential pathways. However, the mechanisms that gut microbiota mediate lipid metabolism in Alzheimer’s disease pathology remain unclear, necessitating further investigation for clarification. This review highlights the current understanding of how gut microbiota disrupts lipid metabolism and discusses the implications of these discoveries in guiding strategies for the prevention or treatment of Alzheimer’s disease based on existing data.

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来源期刊

Molecular Neurodegeneration 医学-神经科学

CiteScore

23.00

自引率

4.60%

发文量

审稿时长

6-12 weeks

期刊介绍： Molecular Neurodegeneration, an open-access, peer-reviewed journal, comprehensively covers neurodegeneration research at the molecular and cellular levels. Neurodegenerative diseases, such as Alzheimer's, Parkinson's, Huntington's, and prion diseases, fall under its purview. These disorders, often linked to advanced aging and characterized by varying degrees of dementia, pose a significant public health concern with the growing aging population. Recent strides in understanding the molecular and cellular mechanisms of these neurodegenerative disorders offer valuable insights into their pathogenesis.