Intermittent fasting and neuroprotection in Alzheimer's disease: metabolic mechanisms, cellular signaling, and brain-peripheral crosstalk.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic, preclinical, and emerging clinical literature without systematic review or meta-analysis.
PubMed 42266620 · doi:10.3389/fnut.2026.1839995
What was done
This narrative review synthesized literature on the mechanistic pathways linking intermittent fasting to neuroprotection in Alzheimer's disease, evaluating preclinical rodent studies and emerging clinical evidence.
What was found
The abstract provides no quantitative metrics or numerical findings. It qualitatively describes that intermittent fasting triggers a metabolic shift toward ketone body production (primarily β-hydroxybutyrate), supports the astrocyte-neuron lactate shuttle, inhibits mTOR signaling to enhance autophagy, reduces microglial activation and neuroinflammation, raises brain-derived neurotrophic factor levels, and modulates peripheral myokine and adipokine signaling to attenuate amyloid-β and tau pathology.
Why it matters
The review outlines how dietary restriction protocols might bypass cerebral glucose hypometabolism and support neuronal resilience in neurodegenerative disease.
Limits
As a narrative review, the paper provides no primary human trial data, effect estimates, sample size counts, or systematic search methodology. The reported therapeutic benefits are derived predominantly from rodent models, and clinical efficacy in human Alzheimer's disease remains unproven.
Cited by
- supports Astrocytes are highly glycolytic and produce lactate from glucose, which is shuttled into neurons as an energy source and acts as a signaling molecule that affects BDNF.