LeeLemonoil
Member
- Joined
- Sep 24, 2016
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Another gem that corrobates much that Peat and Peaters postulate when it comes to depressive disorders, the effects and roles of Tetracyclines and Serotonin/SSRIs in particular.
Publication from 2019:
Minocycline alters behavior, microglia and the gut microbiome in a trait-anxiety-dependent manner - PubMed
Minocycline alters behavior, microglia and the gut microbiome in a trait-anxiety-dependent manner
Abstract
Major depressive disorder is the main cause of disability worldwide with imperfect treatment options. However, novel therapeutic approaches are currently discussed, from augmentation strategies to novel treatments targeting the immune system or the microbiome-gut-brain axis. Therefore, we examined the potential beneficial effects of minocycline, a tetracycline antibiotic with pleiotropic, immunomodulatory action, alone or as augmentation of escitalopram on behavior, prefrontal microglial density, and the gut microbiome in rats selectively bred for high anxiety-like behavior (HAB). We show that concomitant with their high innate anxiety and depression, HABs have lower microglial numbers in the infralimbic and prelimbic prefrontal cortex and an altered gut microbiota composition compared with controls. Three weeks of minocycline treatment alleviated the depressive-like phenotype, further reduced microglial density, exclusively in male HAB rats, and reduced plasma concentrations of pro-inflammatory cytokines. However, coadministration of escitalopram, which had no effect alone, prevented these minocycline-induced effects. Moreover, minocycline led to a robust shift in cecal microbial composition in both HABs and rats non-selected for anxiety-like behavior. Minocycline markedly increased relative abundance of Lachnospiraceae and Clostridiales Family XIII, families known for their butyrate production, with a corresponding increase and positive correlation in plasma 3-OH-butyrate levels in a trait-dependent manner. Thus, our data suggest that the antidepressant effect of minocycline is sex- and trait-dependent, associated with a reduced microglial number in the prefrontal cortex, and with changes in microbial composition and their metabolites. These results further support the microbiome-gut-brain axis as potential target in the treatment of depression.
Someone recently here also posted studies showing that butyrate titers in the blood are a sign or cause of anti-inflammatory general condition or effects.
Note that this is a murine study and also note that this is a short-term intervention. I perosnaly think that long-term adminitration of minocycline is problematic and can result in pro-depressive and pro-inflammatory conditions
Nevertheless, Peat right again
@haidut
Publication from 2019:
Minocycline alters behavior, microglia and the gut microbiome in a trait-anxiety-dependent manner - PubMed
Minocycline alters behavior, microglia and the gut microbiome in a trait-anxiety-dependent manner
Abstract
Major depressive disorder is the main cause of disability worldwide with imperfect treatment options. However, novel therapeutic approaches are currently discussed, from augmentation strategies to novel treatments targeting the immune system or the microbiome-gut-brain axis. Therefore, we examined the potential beneficial effects of minocycline, a tetracycline antibiotic with pleiotropic, immunomodulatory action, alone or as augmentation of escitalopram on behavior, prefrontal microglial density, and the gut microbiome in rats selectively bred for high anxiety-like behavior (HAB). We show that concomitant with their high innate anxiety and depression, HABs have lower microglial numbers in the infralimbic and prelimbic prefrontal cortex and an altered gut microbiota composition compared with controls. Three weeks of minocycline treatment alleviated the depressive-like phenotype, further reduced microglial density, exclusively in male HAB rats, and reduced plasma concentrations of pro-inflammatory cytokines. However, coadministration of escitalopram, which had no effect alone, prevented these minocycline-induced effects. Moreover, minocycline led to a robust shift in cecal microbial composition in both HABs and rats non-selected for anxiety-like behavior. Minocycline markedly increased relative abundance of Lachnospiraceae and Clostridiales Family XIII, families known for their butyrate production, with a corresponding increase and positive correlation in plasma 3-OH-butyrate levels in a trait-dependent manner. Thus, our data suggest that the antidepressant effect of minocycline is sex- and trait-dependent, associated with a reduced microglial number in the prefrontal cortex, and with changes in microbial composition and their metabolites. These results further support the microbiome-gut-brain axis as potential target in the treatment of depression.
Someone recently here also posted studies showing that butyrate titers in the blood are a sign or cause of anti-inflammatory general condition or effects.
Note that this is a murine study and also note that this is a short-term intervention. I perosnaly think that long-term adminitration of minocycline is problematic and can result in pro-depressive and pro-inflammatory conditions
Nevertheless, Peat right again
@haidut
