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Researchers found in a mouse model that time-restricted eating may help manage symptoms of Alzheimer’s disease. Maskot/Getty Images
  • Intermittent fasting, or time-restricted feeding, involves restricting the energy intake to fixed time periods and fasting outside these times.
  • The practice is associated with several health benefits, such as improved sleep, weight control, blood glucose regulation, cardiac function, and gut health.
  • Studies in mice have found that time-restricted feeding may also have anti-aging and anticancer effects.
  • A new study has found that, in a mouse model of Alzheimer’s disease, time-restricted feeding improved memory and reduced Alzheimer’s pathology in the brain.

A recent study in a mouse model suggests that intermittent fasting, or time-restricted eating, may benefit those experiencing symptoms of Alzheimer’s disease (AD).

Alzheimer’s disease — a progressive and ultimately fatal neurodegenerative condition — is the most common form of dementia.

Current treatments can help to alleviate symptoms, such as memory loss, sleep issues, and behavioral problems.

Newer monoclonal antibody drugs — donanemab, aducanumab, and lecanemab — that clear amyloid plaques perform well in trials. However, these are not yet widely available as research is ongoing.

Another approach to alleviating Alzheimer’s disease symptoms relies on lifestyle modifications.

A laboratory study has found that time-restricted feeding corrects the circadian disruptions of Alzheimer’s disease, improves memory, and reduces the accumulation of amyloid — a protein tied to dementia progression — in the brain.

If these effects in mice can be replicated in people, it could be a simple way to help manage Alzheimer’s disease.

The study, from the University of California San Diego School of Medicine, is published in Cell Metabolism.

Dr. Percy Griffin, PhD, Alzheimer’s Association director of scientific engagement, not involved in the research, commented:

“The authors noted that one limitation of the study was the model used. The mouse model only displayed amyloid deposition, which is one of the hallmarks of Alzheimer’s. The model did not display other hallmarks including tau tangle formation [which is another marker of dementia] or brain cell loss. While this is interesting work, we need more research in other models for confirmation.”

Time-restricted feeding or intermittent fasting involves entirely or partially abstaining from eating. Methods include eating within a certain time period each day (time-restricted feeding), or fasting for one or more days a week while eating normally on other days.

Although research in humans is limited, intermittent fasting has been associated with several health benefits, and many studies are currently in progress.

Benefits may include weight loss, reduced risk of type 2 diabetes, improved heart health, reduced risk of some cancers, and improved brain health.

Previous mouse studies have linked time-restricted feeding with gene modification, longevity, and reduced cancer risk. This latest study found that, in mice, time-restricted feeding corrected the circadian disruptions of Alzheimer’s disease.

Circadian disruptions — altered sleep rhythms and difficulty falling or staying asleep — are a common feature of Alzheimer’s disease, often beginning early in the course of the disease.

Research suggests that there is a two-way relationship between circadian disruptions and Alzheimer’s disease pathology, as Dr. Griffin, who was not involved in the study, explained:

“There is an established bidirectional relationship between circadian rhythm dysfunction and neurodegeneration. Changes in circadian rhythms lead to protein accumulation and other changes associated with neurodegeneration. Further, neurodegenerative changes lead to changes in circadian rhythms and dysfunction.”

“The changes in Alzheimer’s and circadian rhythm dysfunction negatively impact each other and more research is needed to firmly establish causality,” he added.

In the new study, the researchers used transgenic mice engineered to develop Alzheimer’s disease pathology and wild-type mice.

They divided the mice randomly into two groups, both of which contained some transgenic and some wild-type mice. All the mice were used to 12 hours of light and 12 of darkness.

The transgenic Alzheimer’s disease mice exhibited sleep disruption and altered activity rhythms, being much more active during the dark phase than the wild-type mice.

One group had constant access to food, and the other had food available for only 6 hours during the 12-hour light phase each day. Despite the difference in food availability, both groups consumed equivalent volumes of food and showed no significant differences in body weight.

As well as taking blood samples from the mice for analysis, the researchers tested their cognitive function using two methods — the novel object recognition test (NOR) and an eight-arm radial arm maze (RAM).

At the end of the experimental period, they euthanized the mice and analyzed their brains to assess changes in gene expression and the extent of amyloid deposition.

Time-restricted feeding decreased blood glucose (sugar) levels in all the mice, and modified gene expression in the Alzheimer’s disease mice, reducing the expression of genes associated with neuroinflammation and regulating clock-controlled genes.

After 3 months, the researchers assessed the impact of time-restricted feeding on behavior in the Alzheimer’s disease mice. They found different effects in males and females, with only females increasing total sleep. Both sexes showed improved sleep onset and reduced hyperactivity.

The Alzheimer’s disease mice on time-restricted feeding exhibited significantly reduced amyloid plaques compared with those on unlimited feeding. The researchers suggest that time-restricted feeding may reduce the amyloid deposition rate and increase the amyloid clearance rate.

The mice on time-restricted feeding also showed improved memory and cognitive function. Before time-restricted feeding, the Alzheimer’s disease mice performed worse than wild-type mice in the NOR and RAM tests.

Following time-restricted feeding, they improved on both tests, whereas the Alzheimer’s disease mice on unlimited food continued to show deficits.

For the Alzheimer’s disease mice on time-restricted feeding, cognitive performance improved to almost the levels of the wild-type mice.

Sebnem Unluisler, a genetic engineer at the London Regenerative Institute, not involved in the study, explained the potential mechanisms behind the changes for Medical News Today.

“Numerous processes may contribute to intermittent fasting’s beneficial effects on Alzheimer’s disease. Autophagy, a cellular process that eliminates damaged components and has been associated with neuroprotection, may be one important mechanism,“ she suggested.

“Intermittent fasting may improve autophagic functions, which could aid in the removal of harmful protein clumps like amyloid-beta, a sign of Alzheimer’s disease,” Unluisler added.

“Furthermore, by encouraging the release of brain-derived neurotrophic factor(BDNF), intermittent fasting may enhance brain function, lower oxidative stress, and enhance metabolic health,” she noted.

Unluisler also commented on the potential to translate these findings from mice to humans. She told us:

“Even though the study was done on mice, and findings from animal studies can be difficult to translate to human studies, it provides a good basis for thinking about how intermittent fasting can affect Alzheimer’s disease in humans. Given the possible advantages of intermittent fasting on metabolic health and neuroprotection, it is logical to speculate that comparable effects would be seen in humans.”

The researchers who conducted the study believe that time-restricted feeding could be an easy way to help alleviate circadian problems in people with Alzheimer’s disease, one of the main causes of them needing residential care.

“Time-restricted feeding is a strategy that people can easily and immediately integrate into their lives,” said senior study author Dr. Paula Desplats, professor in the Department of Neurosciences at UC San Diego School of Medicine.

“If we can reproduce our results in humans, this approach could be a simple way to dramatically improve the lives of people living with Alzheimer’s and those who care for them.”

However, Dr. Griffin urged caution: “More work is needed — both in models and in people — before this approach can be recommended broadly as a strategy for reducing the risk of neurodegeneration.”