Epigenetics in depression and gut-brain axis: A molecular crosstalk

Published on December 13, 2022

Think of your gut and brain as two best friends who never stop talking to each other. They have their own secret language called the gut-brain axis, a communication network that plays a crucial role in our well-being. This axis can go haywire, leading to all sorts of problems including depression. How does this happen? Well, it turns out that the bacteria in your gut, collectively known as the gut microbiota, have a direct line to your brain. They can change your brain’s chemistry by producing certain molecules that can affect your genes, like invisible puppet masters controlling your DNA strings! These molecules can regulate the activity of your genes through a process called epigenetic modification, which involves chemical changes to your DNA and its surrounding proteins. Scientists have found that imbalances in the gut microbiota and epigenetic changes are closely linked to depression. By understanding how the gut-brain axis and epigenetics work together in depression, we may be able to find new ways to diagnose, prevent, and treat this debilitating condition. For more mind-blowing details, check out the full article!

Gut-brain axis is a dynamic, complex, and bidirectional communication network between the gut and brain. Changes in the microbiota-gut-brain axis are responsible for developing various metabolic, neurodegenerative, and neuropsychiatric disorders. According to clinical and preclinical findings, the gut microbiota is a significant regulator of the gut-brain axis. In addition to interacting with intestinal cells and the enteric nervous system, it has been discovered that microbes in the gut can modify the central nervous system through metabolic and neuroendocrine pathways. The metabolites of the gut microbiome can modulate a number of diseases by inducing epigenetic alteration through DNA methylation, histone modification, and non-coding RNA-associated gene silencing. Short-chain fatty acids, especially butyrate, are well-known histone deacetylases inhibitors. Similarly, other microbial metabolites such as folate, choline, and trimethylamine-N-oxide also regulate epigenetics mechanisms. Furthermore, various studies have revealed the potential role of microbiome dysbiosis and epigenetics in the pathophysiology of depression. Hence, in this review, we have highlighted the role of gut dysbiosis in epigenetic regulation, causal interaction between host epigenetic modification and the gut microbiome in depression and suggest microbiome and epigenome as a possible target for diagnosis, prevention, and treatment of depression.

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