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Controlled calories and low-fat diet may protect an aging brain, study shows

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Algemeen advies 12/03/2018 11:55
12 Mar 2018 --- Following a low-fat diet in combination with limited caloric consumption can prevent age-related brain dysfunction in aging mice. The study, published in Frontiers in Molecular Neuroscience, also finds that exercise is far less effective than the caloric restriction in preventing such neurological, age-related changes. Although an early day’s rodent study, this data could demonstrate the potential importance of dietary fat intake on brain health in aging populations.

“Obesity and aging are both prevalent and increasing in societies worldwide, but the consequences for the central nervous system are not well understood,” says Bart Eggen, lead author of the study and a researcher at the University Medical Center Groningen in the Netherlands. “We determined if a high- or low-fat diet, in combination with exercise and food restriction, impacted microglia during aging in mice.”

Microglia are brain cells that help maintain healthy function of the brain. Dysfunction of these cells, as may occur in disease, is linked to neurodevelopmental disorders and neurodegenerative conditions.

The aging process is also associated with inflammation caused by microglia in some regions of the brain, but it is unclear whether diet and lifestyle can influence this process.

The study sought to find the impact of high-and low-fat diets on inflammation and microglial markers in the hypothalamus of six-month-old mice. Furthermore, they also looked at the effects of these diets on two-year-old mice. These mice either followed a lifelong exercise regime or a lifelong calorie restricted diet.

“Aging-induced inflammatory activation of microglia could only be prevented when mice were fed a low-fat diet in combination with limited caloric intake," says Eggen. "A low-fat diet per se was not sufficient to prevent these changes.”

Limitations and future implications
Eggen points out that further research is needed to thoroughly understand the meaning of the findings. For example, what could the effects be of numerous diet-types during a lifetime, or even swapping between diets during a lifetime? It also remains unclear whether switching to a low-fat, calorie restricted diet could undo the negative consequences of a high-fat, high-calorie diet.

“Nevertheless, these data do show that, in mice, the fat content of a diet is an important parameter in terms of the detrimental effects of aging on the brain, as well as caloric intake. Only when fat content and caloric intake are limited, can aging-induced changes in microglia be prevented,” concluded Eggen.

As well as having similar genome patterns to humans, the mouse has a short lifespan, which means scientists can easily measure the effects of aging (one mouse year equals about thirty human years), according to The National Human Genome Institute.

Therefore, this rodent study may only add early or preliminary findings to this particular knowledge field but, the data could aid essential future additions to knowledge linking diet, caloric intake and brain health.

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