Intermittent fasting and neuroprotection in Alzheimer’s disease: metabolic mechanisms, cellular signaling, and brain-peripheral crosstalk (opens in new tab)

Intermittent fasting (IF) promotes a metabolic switch characterized by reduced glucose and insulin availability along with increased lipolysis and ketone body production, particularly β-hydroxybutyrate (βOHB). In the brain, IF enhances metabolic flexibility by facilitating ketone utilization and supporting the astrocyte–neuron lactate shuttle (ANLS), partially compensating for cerebral glucose hypometabolism which is commonly observed in Alzheimer’s disease (AD). Beyond bioenergetics, IF acti...