Mechanisms of time-restricted feeding-induced neuroprotection and neuronal plasticity in ischemic stroke as a function of circadian rhythm.
Abstract
Time-restricted feeding (TRF) is known to promote longevity and brain function, and potentially prevent neurological diseases. Animal studies show that TRF enhances brain-derived neurotrophic factor (BDNF) signaling and regulates autophagy and neuroinflammation, supporting synaptic plasticity, neurogenesis and neuroprotection. Feeding/fasting paradigms influence the circadian cycle, with TRF aligning circadian cycle-related gene expression, and thus altering physiological processes. Emerging evidence highlights the role of gut microbiota in neuronal plasticity, based on the observation that TRF significantly alters gut microbiota composition. Hence, the gut-brain axis may be crucial for maintaining cognitive functions and presents a potential therapeutic target for TRF-mediated neuroprotection. In the context of ischemic stroke where neuronal damage is extensive, TRF can be a preconditioning strategy to enhance synaptic plasticity and neuronal resilience, thus improving outcomes after stroke. This review discussed the link between TRF and circadian regulation in neuronal plasticity and its implications for recovery after stroke.
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Research summary
The paper discusses time-restricted feeding (TRF) and its potential neuroprotective effects, which could relate to longevity through mechanisms like synaptic plasticity and neurogenesis. However, while it touches on aspects of aging and neurological health, it primarily focuses on the effects of TRF in the context of ischemic stroke rather than addressing the root causes of aging or lifespan extension directly. The findings are solid but do not present a significant breakthrough or transformative implications for the field of longevity research.
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