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Dcf1 deletion presents alterations in gut microbiota of mice similar to Parkinson’s disease

The gut-brain communication is increasingly being recognized as a profound effector on Parkinson’s disease (PD). Gut microbiota changes have become the focus of attention. However, the mechanism leading to changes in the gut microbiota is not clear. In the present study, we found that knockout of Dc...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2020-09, Vol.529 (4), p.1137-1144
Main Authors: Li, Weihao, Zhao, Qinpin, Wang, Jiao, Wang, Yajiang, Wen, Tieqiao
Format: Article
Language:English
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Summary:The gut-brain communication is increasingly being recognized as a profound effector on Parkinson’s disease (PD). Gut microbiota changes have become the focus of attention. However, the mechanism leading to changes in the gut microbiota is not clear. In the present study, we found that knockout of Dcf1 (Dcf1−/−) caused changes in the gut microbiota in mice. Results indicated that the increased Proteobacteria (phylum-level) and decreased Prevotellaceae (family-level) in the microbiota composition of Dcf1−/− (KO) mice, which is consistent with the situation of PD patients. On species-level, Prevotellaceae_UCG-001 and Helicobacter_ganmani were significantly different between KO and WT mice, suggesting glycolipid metabolism disorders and inflammatory lesions in KO mice. In the behavior of Y-maze and Open field test, KO mice showed typical PD symptoms such as memory deficits, slowness of movement and anxiety. Further Nissl staining of brain tissue sections confirmed that the deletion of Dcf1 caused damage to amygdala neurons. These results provide a new mechanism for understanding gut microbiota changes, and provide a new basis for PD treatment from a new perspective of Gut-brain axis. •Dcf1 deletion causes changes in mice gut microbiota.•The changes of gut microbiota in Dcf1 knockout mice is similar to that of PD clinical microbiota.•Dcf1 knockout mice show PD-like behavior and pathology.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2020.06.150