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Title: Altered gut microbial metabolites in amnestic mild cognitive impairment and alzheimer's disease : signals in host-microbe interplay
Authors: Wu, Li
Han, Yuqiu
Zheng, Zhipeng
Peng, Guoping
Liu, Ping
Yue, Siqing
Zhu, Shuai
Chen, Jun
Lv, Hanying
Shao, Lifang
Sheng, Yan
Wang, Yulan
Li, Liang
Li, Lanjuan
Wang, Baohong
Keywords: Science::Medicine
Issue Date: 2021
Source: Wu, L., Han, Y., Zheng, Z., Peng, G., Liu, P., Yue, S., . . . Wang, B. (2021). Altered Gut Microbial Metabolites in Amnestic Mild Cognitive Impairment and Alzheimer’s Disease: Signals in Host–Microbe Interplay. Nutrients, 13(1), 228-. doi:10.3390/nu13010228
Journal: Nutrients
Abstract: Intimate metabolic host-microbiome crosstalk regulates immune, metabolic, and neuronal response in health and disease, yet remains untapped for biomarkers or intervention for disease. Our recent study identified an altered microbiome in patients with pre-onset amnestic mild cognitive impairment (aMCI) and dementia Alzheimer's disease (AD). Thus, we aimed to characterize the gut microbial metabolites among AD, aMCI, and healthy controls (HC). Here, a cohort of 77 individuals (22 aMCI, 27 AD, and 28 HC) was recruited. With the use of liquid-chromatography/gas chromatography mass spectrometry metabolomics profiling, we identified significant differences between AD and HC for tryptophan metabolites, short-chain fatty acids (SCFAs), and lithocholic acid, the majority of which correlated with altered microbiota and cognitive impairment. Notably, tryptophan disorders presented in aMCI and SCFAs decreased progressively from aMCI to AD. Importantly, indole-3-pyruvic acid, a metabolite from tryptophan, was identified as a signature for discrimination and prediction of AD, and five SCFAs for pre-onset and progression of AD. This study showed fecal-based gut microbial signatures were associated with the presence and progression of AD, providing a potential target for microbiota or dietary intervention in AD prevention and support for the host-microbe crosstalk signals in AD pathophysiology.
ISSN: 2072-6643
DOI: 10.3390/nu13010228
Rights: © 2021 The Authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:LKCMedicine Journal Articles

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