微生物组在神经退行性疾病中的潜在贡献:阿尔茨海默病

R. Kumari, Nirmal Verma, J. Paul
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引用次数: 3

摘要

阿尔茨海默病(AD)的特点是认知和记忆的缓慢进行性下降,是痴呆症的最常见原因。HM参与多种神经化学和神经代谢途径的调节。阿尔茨海默病的病理特征包括淀粉样肽(Aβ)沉积、神经元缠结形成和颗粒空泡变性。a β蛋白是先天免疫系统的正常组成部分,是人体抵御感染的第一道防线。然而,最近的报告显示,在AD的小鼠、线虫和细胞培养模型中,Ab表达对真菌和细菌感染有保护作用。然而,最近的研究表明,这些蛋白质也在细菌和真菌细胞表面表达,并可能有助于免疫反应。除了共生微生物外,其他病原体如肺炎衣原体、刚地弓形虫、HIV相关神经认知障碍(HAND)、类病毒、肝炎、巨细胞病毒等也被怀疑与AD有关。微生物通过产生相关的神经递质水平、过度炎症引起的免疫调节以及从感染部位通过血液或淋巴系统转运到大脑的能力,被认为参与了神经退行性疾病的病理生理。在这里,我们详细阐述了新兴的观点,显示肠道微生物群对人类神经系统疾病的贡献,特别强调AD。本文概述的证据可能有助于设计进一步的研究,以进行AD患者微生物群的分类和功能分析,从而导致新的先进治疗发明。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Potential Contribution of Microbiome In Neurodegenerative Diseases: Alzheimer's Disease
Alzheimer’s Disease (AD) is characterized by a slowly progressive decline of cognition and memory and is the most frequent cause of dementia. HM contribute to the regulation of multiple neuro-chemical and neuro-metabolic pathways. The pathological features of AD include amyloid beta peptide (Aβ) deposition, neuronal tangle formation and granulovacuolar degeneration. Aβ protein is a normal part of the innate immune system, the body's first-line defense against infection. However recent report shows that Ab expression protects against fungal and bacterial infections in mouse, nematode, and cell culture models of AD.   However, recent research has shown that these proteins are also expressed on bacterial and fungal cell surfaces and might contribute to immune response.  In addition to commensal microbes there are other pathogens like Chlamydophila pneumoniae, Toxoplasma gondii, HIV- associated neurocognitive disorders (HAND, Viroids, Hepatitis, Cytomegalovirus have been suspected to be involved in AD.  Microbes are proposed to be involved in pathophysiology of neurodegenerative disease through their ability to produce relevant neurotransmitter level, immune modulation due to excess inflammation and translocation to brain from the site of infection trough blood or lymphatic system. Here we elaborated on the emerging ideas showing the contribution of the gut microbiome to human neurological diseases with special emphasis on AD. The evidences outlined in this review may prove useful in designing further studies for taxonomic and functional profiling of microbiota in patients with AD leading to new advanced therapeutic inventions.
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