Intermittent Fasting (IF/TRE) for Alzheimer's Disease
Also known as: IF, Time-restricted eating, TRE, 16:8 fasting, 5:2 diet
Intermittent fasting activates autophagy and ketogenesis — two processes that clear amyloid aggregates and provide alternative neuronal fuel.
Mechanism of Action
Fasting activates AMPK and inhibits mTOR, inducing autophagy for Aβ and tau clearance. Hepatic ketogenesis provides BHB as alternative fuel for glucose-hypometabolic AD neurons. Fasting also activates SIRT1/3 and reduces insulin/IGF-1 signaling implicated in AD pathogenesis.
General mechanism: Temporal caloric restriction. AMPK activation, mTOR inhibition, autophagy induction, SIRT1 activation, ketogenesis, differential stress resistance.
Current Evidence
Preclinical models show improved cognition and reduced pathology with IF. Human studies show improved insulin sensitivity and metabolic biomarkers. AD-specific RCTs are in early stages.
Clinical Status: Preclinical positive. Metabolic biomarker studies in humans supportive. AD trials emerging.
Safety Profile
Generally safe for healthy individuals. Contraindicated in eating disorders. ALS: caloric maintenance critical. Diabetics: medication adjustment needed.
Key Research Questions
- Can TRE improve brain insulin sensitivity in AD patients?
- Does fasting-induced autophagy clear amyloid aggregates in human brain?