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J Alzheimers Dis. 2019 Jun 4. doi: 10.3233/JAD-181220. [Epub ahead of print]

Gut Microbiota Alteration and Its Time Course in a Tauopathy Mouse Model.

Author information

1
Department of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, China.
2
State Key Laboratory of Trauma, Burn and Combined Injury, Third Military Medical University, Chongqing, China.
3
Centre for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Science, Beijing, China.

Abstract

Emerging evidence suggests that gut microbiota dysbiosis plays a role in neurodegenerative disorders. However, whether the composition and diversity of the gut microbiota are altered in tauopathies remains largely unknown. This study was aimed to examine the diversity and composition of the gut microbiota in tauopathies, as well as the correlation with pathological changes in the brain. We collected fecal samples from 32 P301L tau transgenic mice and 32 age- and gender-matched littermate mice at different ages. The 16S ribosomal RNA sequencing technique was used to analyze the microbiota composition in feces. Brain tau pathology levels were measured by immunohistochemistry. The diversity and composition of the gut microbiota significantly changed with aging. At the phylum level, the relative abundance of Bacteroidetes was increased, while Firmicutes were decreased in P301L mice compared with that in Wt mice after 3 months of age. In addition, Actinobacteria was decreased in P301L mice at 3 and 6 months of age, meanwhile Tenericutes was decreased in P301L mice at 10 months of age. Moreover, several specific macrobiota were highly associated with the levels of paired helical filament-tau or pT231-tau protein in the brain. Our findings suggest that gut microbiota changed with aging, as well as in the tauopathy mice model. Modulation of the gut microbiota may be a potential strategy for treatment of tauopathy.

KEYWORDS:

16S ribosomal RNA sequencing; gut microbiota; tau; tauopathy

PMID:
31177213
DOI:
10.3233/JAD-181220

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