This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research
Diling Chen
Guangdong Institute of Microbiology
Corresponding Author
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: The gut-brain axis has been implicated in the complex pathogenesis of Alzheimer’s disease (AD), but the action is unclear, this study was performed to clarify the effect of ad-related gut microbiota on the pathogenesis of AD during pregnancy and early exposure.
Methods: A pilot study of gut microbiota in AD patients was performed.
Gut microbiota structure, long-term potentiation (LTP), inflammation levels, AD biomarkers, and metabolomics of serum and fecal were monitored after cohousing by cohousing in early life (from pregnancy 14 days to birth 14 days with 8-month old APP/PS1 mice).The regulatory action of bacterial metabolites on Tau protein phosphorylation was evaluated.
Results: Gut microbiota from APP/SP1 mice altered structure of gut microbiota in newborn mice, LTP in hippocampal slices was significantly shortened, and inflammatory markers levels were increased, AD biomarkers were upregulated, with significantly higher Tau protein phosphorylation at multiple sites (p < 0.05).
Conclusions: These results imply ad-related gut microbiota can change the structure of gut microbiota during pregnancy and early exposure. Changing the structure of gut microbiota in the newborn mice can induce leucine metabolism disorder, induce mTOR mediated autophagy dysfunction and increase the level of inflammation, thus leading to accelerate Tau protein phosphorylation and reduce LTP occurs in AD-cohousing mouse hippocampus.
Keywords
Alzheimer’s disease, Gut microbiota, Fecal microbiota transplantation, Tau protein hyperphosphorylation, Gut-brain axis
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
Figure 8
Figure 9
This is a list of supplementary files associated with this preprint. Click to download.
Loading...
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 09 Jun, 2020
Community comments: 1
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cognitive Neuroscience
Learn more about our company.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research
Diling Chen
Guangdong Institute of Microbiology
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 09 Jun, 2020
Community comments: 1
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cognitive Neuroscience
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: The gut-brain axis has been implicated in the complex pathogenesis of Alzheimer’s disease (AD), but the action is unclear, this study was performed to clarify the effect of ad-related gut microbiota on the pathogenesis of AD during pregnancy and early exposure.
Methods: A pilot study of gut microbiota in AD patients was performed.
Gut microbiota structure, long-term potentiation (LTP), inflammation levels, AD biomarkers, and metabolomics of serum and fecal were monitored after cohousing by cohousing in early life (from pregnancy 14 days to birth 14 days with 8-month old APP/PS1 mice).The regulatory action of bacterial metabolites on Tau protein phosphorylation was evaluated.
Results: Gut microbiota from APP/SP1 mice altered structure of gut microbiota in newborn mice, LTP in hippocampal slices was significantly shortened, and inflammatory markers levels were increased, AD biomarkers were upregulated, with significantly higher Tau protein phosphorylation at multiple sites (p < 0.05).
Conclusions: These results imply ad-related gut microbiota can change the structure of gut microbiota during pregnancy and early exposure. Changing the structure of gut microbiota in the newborn mice can induce leucine metabolism disorder, induce mTOR mediated autophagy dysfunction and increase the level of inflammation, thus leading to accelerate Tau protein phosphorylation and reduce LTP occurs in AD-cohousing mouse hippocampus.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
Figure 8
Figure 9
This is a list of supplementary files associated with this preprint. Click to download.
Loading...