RESUMO
OBJECTIVE: Caloric restriction by intermittent fasting produces several metabolic changes, such as increased insulin sensitivity and use of ketone bodies as energy sources. In humans, intermittent fasting has been studied in hypertension, diabetes, and related conditions, but, to date, not as a strategy to reduce the risk of emergent dementia. In this scoping review, the relevance of intermittent fasting as a potential preventive intervention for Alzheimer's dementia is explored. BACKGROUND: The beneficial effects of calorie restriction have been documented in animals and humans. Decreased oxidative stress damage and attenuated inflammatory responses are associated with intermittent fasting. These changes have a favorable impact on the vascular endothelium and stress-induced cellular adaptation. RESULTS: Physiological alterations associated with fasting have profound implications for pathological mechanisms associated with dementias, particularly Alzheimer's disease. Compared with ad libitum feeding, caloric restriction in animals was associated with a reduction in ß-amyloid accumulation, which is the cardinal pathological marker of Alzheimer's disease. Animal studies have demonstrated synaptic adaptations in the hippocampus and enhanced cognitive function after fasting, consistent with these theoretical frameworks. Furthermore, vascular dysfunction plays a crucial role in Alzheimer's disease pathology, and intermittent fasting promotes vascular health. CONCLUSIONS: These observations lead to a hypothesis that intermittent fasting over the years will potentially reverse or delay the pathological process in Alzheimer's disease.
