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• W2894075596 abstract "Growing evidence link gut microbiome to the development and maturation of the central nervous system, which are regulated by microbiota potentially through stress response, neurotransmitter, neuroimmune, and endocrine pathways. The dysfunction of such microbiota-gut-brain axis is implicated in neuropsychiatric disorders, depression, and other stress-related conditions. Using affective disorders as our primary outcomes, we inspect the current evidence of microbiota studies mainly in human clinical samples. Additionally, to restore microbiome equilibrium in bacteria diversity and abundance might represent a novel strategy to prevent or treat mood symptoms. We reviewed findings from clinical trials regarding efficacy of probiotics supplement with or without antidepressant treatment, and adjuvant antimicrobiotics treatment. In microbiota studies, the considerations of host-microbiota interaction and bacteria-bacteria interaction are discussed. In conclusion, the roles of microbiota in depression and mania state are not fully elucidated. One of the challenges is to find reliable targets for functional analyses and experiments. Notwithstanding some inconsistencies and methodological limitations across studies, results from recent clinical trials support for the beneficial effects of probiotics on alleviating depressive symptoms and increasing well-beings. Moreover, modifying the composition of gut microbiota via antibiotics can be a viable adjuvant treatment option for individuals with depressive symptoms." @default.
• W2894075596 created "2018-10-05" @default.
• W2894075596 creator A5011953626 @default.
• W2894075596 creator A5047251323 @default.
• W2894075596 date "2019-03-01" @default.
• W2894075596 modified "2023-09-25" @default.
• W2894075596 title "Moody microbiome: Challenges and chances" @default.
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• W2894075596 doi "https://doi.org/10.1016/j.jfma.2018.09.004" @default.
• W2894075596 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30262220" @default.
• W2894075596 hasPublicationYear "2019" @default.
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