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Post-stroke depression: epigenetic and epitranscriptomic modifications and their interplay with gut microbiota.
Soomin Jeong1,2, Anil K Chokkalla1, Charles K Davis1
1Department of Neurological Surgery, University of Wisconsin, Madison, WI, USA.
Molecular Psychiatry
|May 15, 2023
Summary
Gut microbiota influences epigenetic and epitranscriptomic changes, impacting stroke and depression. Targeting these pathways, including specific genes, offers novel therapeutic strategies for post-stroke depression.
Area of Science:
- Neuroscience
- Microbiology
- Genetics
Background:
- Epigenetic and epitranscriptomic modifications regulate physiological processes at DNA and RNA levels.
- Gut microbiota and its metabolites influence epigenetic (DNA methylation, histone modification) and epitranscriptomic (N6-methyladenosine) pathways.
- These dynamic modifications are implicated in the pathogenesis of stroke and depression.
Purpose of the Study:
- To review the interplay between gut microbiota, epigenetic/epitranscriptomic pathways, and candidate genes in post-stroke depression.
- To identify novel molecular targets for managing post-stroke depression due to a lack of specific interventions.
Main Methods:
- Literature review focusing on the interaction between gut microbiota and epigenetic/epitranscriptomic modifications.
- Analysis of candidate genes involved in post-stroke depression pathogenesis.
- Focus on brain-derived neurotrophic factor, ten-eleven translocation family proteins, and fat mass and obesity-associated protein.
Main Results:
- Gut microbiota modulates epigenetic and epitranscriptomic modifications.
- These modifications play a role in the development of stroke and depression.
- Specific genes like BDNF, TET, and FTO are implicated in post-stroke depression.
Conclusions:
- The gut microbiota-epigenetics-epitranscriptomics axis is a promising area for novel therapeutic strategies in neurological diseases.
- Understanding this axis can lead to targeted interventions for post-stroke depression.
- BDNF, TET proteins, and FTO are key candidates for further investigation in post-stroke depression.
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