Anti-Oxidant and Anti-Inflammatory Activity of Ketogenic Diet: New Perspectives for Neuroprotection in Alzheimer's Disease.
Level 5 - mechanism / opinion, no new human data
Narrative review of proposed biological mechanisms without systematic synthesis or new empirical data.
PubMed 29710809 · doi:10.3390/antiox7050063
What was done
This paper provides a narrative review summarizing the biochemical mechanisms through which the ketogenic diet and its primary ketone body, beta-hydroxybutyrate, may exert antioxidant and anti-inflammatory neuroprotection in Alzheimer's disease.
What was found
The abstract reports no quantitative clinical or experimental data. It highlights several proposed molecular actions of beta-hydroxybutyrate: reducing reactive oxygen species production, enhancing mitochondrial respiration, activating the endogenous antioxidant transcription factor Nrf2, modulating the NAD+/NADH ratio, increasing electron transport chain efficiency via uncoupling proteins, and exerting anti-inflammatory effects through inhibition of NF-kB, the NLRP3 inflammasome, and histone deacetylases.
Why it matters
It maps the theoretical and preclinical rationale for testing ketogenic nutritional interventions to target mitochondrial dysfunction and neuroinflammation in Alzheimer's disease pathology.
Limits
The abstract describes a non-systematic mechanistic review presenting no direct clinical trial results, human effect sizes, or quantitative outcome measures. Clinical efficacy in human Alzheimer's disease cannot be determined from these mechanistic summaries alone.
Cited by
- supports Initiating a ketogenic diet acts as a physiological stressor that activates the Nrf2 signaling pathway.