About this Research Topic
This Research topic focused on the mechanisms of action of the ketogenic diet aims at collecting recent discoveries centered on elucidating the cellular and molecular mechanisms induced by the ketogenic diet or ketone supplements on neural physiology and possibly, on metabolic and cognitive functions. The main objective is to compile the biological evidence available to support the implementation of the KD in the treatment of specific symptoms or particular diseases, with the goal of supporting targeted usage for better beneficial results.
We are particularly interested in recent discoveries using the KD that tackle the interplay between two or more of the following: metabolism, inflammation, and microbiome. We are interested in results collected in healthy as well as disease conditions, in humans or animal models, that allow a deeper understanding of the cellular pathways directly affected by the diet or the supplements. We seek Original Research, Review, Mini-Review, Hypothesis and Theory, Perspective, Clinical Trial, Case Report and Opinion articles that cover, but are not limited to, the following topics:
- How does the KD induce metabolic changes in the brain and peripheral organs
- What effects KD-induced metabolic changes have on downstream pathways
- How KD-induced downstream effects are related to inflammation
- How KD affects neuroinflammation and neural populations
- How diet-induced microbiome changes might affect systemic and neuroinflammation
- How diet-induced microbiome changes might affect brain health
- How does the KD modulate the interplay between metabolism, neuroinflammation and/or microbiome composition
Keywords: neuroinflammation, NAD+, microbiome, gut-brain axis
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.