Time-restricted eating in Alzheimer's disease (TREAD): A call for research

Apr 6, 2026Journal of Alzheimer's disease : JAD

Time-Restricted Eating and Its Potential in Alzheimer's Disease: A Research Invitation

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Abstract

Delaying progression from mild cognitive impairment to dementia by one year could reduce dementia prevalence by millions.

Intermittent fasting, particularly time-restricted eating, is associated with potential benefits for Alzheimer's disease.
Alzheimer's disease is characterized by specific brain changes, including plaques and neuronal loss, and currently lacks effective pharmacological treatments.
Fasting for at least 8-12 hours may trigger a metabolic shift from glucose to ketone utilization, which could benefit Alzheimer's-affected brains.
Preclinical studies indicate that time-restricted eating may improve cognitive function through mechanisms like neurogenesis and reduced neuroinflammation.
Human studies on time-restricted eating in mild cognitive impairment are limited, primarily focusing on cardiometabolic health rather than cognitive outcomes.

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Fasting is part and parcel of the practice of various religious groups. In the scientific literature, the term intermittent fasting (IF) was first reported in a 1946 paper demonstrating its association with increased longevity in rodents. Research has extended IF, particularly time-restricted eating (TRE), to Alzheimer's disease (AD), a progressive neurodegenerative disease characterized by neuritic plaques, neurofibrillary tangles, and neuronal loss. AD manifests in asymptomatic, mild cognitive impairment (MCI), and dementia phases. Delaying progression from MCI to dementia by one year could reduce dementia prevalence by millions. Currently, no pharmacological treatments can reverse or arrest MCI progression to dementia, making exploration of non-pharmacological interventions critical. TRE is a promising approach. AD brains exhibit decreased glucose uptake, while ketone utilization remains intact. Fasting for at least 8-12 h induces a cascade of molecuar events that lead to a metabolic switch from glucose to ketone utilization, providing an alternative energy source for AD brains. Preclinical studies demonstrate that TRE enhances cognitive function via hippocampal neurogenesis, autophagy, and reduced neuroinflammation. Human studies on TRE in MCI are limited but promising, often focusing on cardiometabolic outcomes, with little known about TRE targeting MCI. This review synthesizes current evidence on TRE and cognitive outcomes in humans, non-human primates, and rodents, and describes ongoing trials in MCI patients. We propose a theoretical model of direct and indirect pathways linking TRE with resistance to AD in the brain parenchyma, and identify gaps in knowledge regarding long-term cognitive effects and mechanistic pathways of TRE in MCI, urging rigorous clinical trials to establish TRE as a safe and possibly effective strategy to delay MCI progression to dementia.

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Time-restricted eating in Alzheimer's disease (TREAD): A call for research

Abstract

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