期刊
CELL REPORTS
卷 34, 期 9, 页码 -出版社
CELL PRESS
DOI: 10.1016/j.celrep.2021.108807
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资金
- Engineering and Physical Sciences Research Council (EPSRC) [EP/S001301/1]
- Biotechnology Biological Sciences Research Council (BBSRC) [BB/S016899/1]
- Science for Life Laboratory
- BBSrC Institute Strategic Programme Gut Microbes and Health [BB/r012490/1, BBS/e/F/000Pr10355]
- Swedish National Infrastructure for Computing at SNIC through Uppsala Multidisciplinary Center for Advanced Computational Science (UPPMAX) [SNIC 2019/3-226, SNIC 2020/5-222]
- IPSEN Pharma Germany
- Merz Pharmaceuticals Germany
- ParkinsonFonds Deutschland gGmbH
- Hilde Ulrich Stiftung for Parkinson's Research, Germany
- BBSRC [BB/S016899/1] Funding Source: UKRI
- EPSRC [EP/S001301/1] Funding Source: UKRI
Parkinson's disease (PD) is a common progressive neurological disorder that affects motor functions, with gastrointestinal (GI) dysfunction being an early nonmotor symptom. This study used metagenomics and serum metabolomics to investigate the gut microbiome of PD patients. The findings suggest that gut microbial composition and metabolism may play a role in PD pathophysiology.
Parkinson's disease (PD) is the most common progressive neurological disorder compromising motor functions. However, nonmotor symptoms, such as gastrointestinal (GI) dysfunction, precede those affecting movement. Evidence of an early involvement of the GI tract and enteric nervous system highlights the need for better understanding of the role of gut microbiota in GI complications in PD. Here, we investigate the gut microbiome of patients with PD using metagenomics and serum metabolomics. We integrate these data using metabolic modeling and construct an integrative correlation network giving insight into key microbial species linked with disease severity, GI dysfunction, and age of patients with PD. Functional analysis reveals an increased microbial capability to degrade mucin and host glycans in PD. Personalized community-level metabolic modeling reveals the microbial contribution to folate deficiency and hyperhomo-cysteinemia observed in patients with PD. The metabolic modeling approach could be applied to uncover gut microbial metabolic contributions to PD pathophysiology.
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