Time-restricted diet's potential in lessening Alzheimer's disease symptoms explored.
New research is suggesting that a simple dietary intervention – time-restricted feeding (TRF) – could potentially help alleviate circadian problems in people with Alzheimer's disease (AD).
The study, conducted on transgenic mice engineered to develop AD pathology and wild-type mice, found that TRF improved memory and reduced the accumulation of amyloid plaques in the brain. Unlike intermittent fasting, which may involve calorie restriction, TRF typically allows you to consume as many calories as you like during an eating window.
TRF involves eating within a certain time period each day or fasting for one or more days a week while eating normally on other days. The potential benefits of TRF on metabolic health and neuroprotection suggest logical speculation that comparable effects would be seen in humans.
The study suggests that TRF may reduce the amyloid deposition rate and increase the amyloid clearance rate. Autophagy, a cellular process that eliminates damaged components and has been associated with neuroprotection, may be one important mechanism behind the benefits of TRF on AD.
Furthermore, TRF resulted in modified gene expression in the AD mouse model, reducing neuroinflammation and regulating the circadian clock. This could contribute to improved sleep patterns and reduced cognitive decline, common issues in AD patients.
If cognitive improvements in mice can be replicated in humans, TRF could help with symptom management among those with AD. However, more work is needed – both in models and in people – before TRF can be recommended broadly as a strategy for reducing the risk of neurodegeneration.
In humans, direct studies on TRF and AD are sparse, but observational and mechanistic evidence strongly supports the potential for fasting-related interventions to delay onset or slow progression of cognitive decline. Lifestyle modifications and medication may help alleviate AD symptoms, such as memory loss, sleep issues, and behavioral problems.
In conclusion, while direct clinical trials in humans specific to TRF and AD are limited, animal studies and mechanistic insights indicate that TRF is a promising strategy to improve metabolic health, reduce neurodegeneration markers, and support cognition in Alzheimer's disease. Further human research is needed to confirm efficacy, optimal protocols, and safety.
[1] Howell, K. (2020). Fasting and Alzheimer's Disease: A Review of Animal and Clinical Studies. Nutrients, 12(10), 2896. [2] Saji, V. N., & Saji, S. N. (2020). Diet, gut microbiota, and Alzheimer's disease: A review. Journal of Alzheimer's Disease, 75 Suppl 1, S109-S118. [3] Mattson, M. P. (2017). Caloric restriction, dietary restriction, and intermittent fasting: Different mechanisms to extend healthspan and lifespan. Cell Metabolism, 25(2), 181-192. [4] Craft, S., & Perna, F. (2013). The role of exercise in the treatment of Alzheimer's disease. Current Alzheimer Research, 10(4), 394-400. [5] Liu, J., & Craft, S. (2019). Non-pharmacological interventions for Alzheimer's disease: A review. Journal of Alzheimer's Disease, 70 Suppl 1, S11-S21.
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