19 September 2006

Low-energy diet good for the brain

A reduced calorie diet could delay the onset of Alzheimer’s disease, found a Mount Sinai School of Medicine study conducted on primates.

A reduced calorie diet could delay the onset of Alzheimer’s disease, found a Mount Sinai School of Medicine study conducted on primates – results that suggest healthy eating not only benefits the waistline but also cognitive functions.

The study, which is set for publication in November’s Journal of Alzheimer's Disease, assesses the potentially beneficial role of calorie restriction in Alzheimer’s-type brain neuropathology in non-human primates.

If restricting caloric intake can in fact prevent Alzheimer’s symptoms by triggering activity in the brain associated with longevity, the findings can only further help the nutraceutical industry as it banks on the success of eating as means of preventing disease.

"This new breakthrough brings great anticipation for further human study of caloric restriction…," said lead author Dr Giulio Maria Pasinetti, director of the Neuroinflammation Research Center at Mount Sinai. "The findings offer a glimmer of hope that there may someday be a way to prevent and stop this devastating disease in its tracks."

The authors took the study on board following previous studies on the link between caloric reduction and Alzheimer’s disease using mouse models. They wanted to take research one step closer to humans, using primates.

The research study
The study was conducted using brain tissue from six male squirrel monkeys: three of which were fed the equivalent of 70 percent the caloric intake of the three in the control group. The monkeys were kept on these diets throughout their entire lifespan until they died of natural causes.

The researchers found that an approximately 30 percent calorie reduction resulted in reduced Alzheimer’s-type amyloid neuropathology in the temporal cortex relative to control fed monkeys.

A variety of proteins are found in the plaques that develop in memory-related areas of the brain as Alzheimer’s develops. Amyloids are insoluble protein masses thought to be involved in the disease. In the study, the decreased Alzheimer’s-type neuropathology correlated with increased longevity of related protein SIRT1, located in the same part of the brain.

“We found that SIRT1 protein expression is elevated in the brain of squirrel monkeys in response to calorie restriction,” wrote the study authors. The SIRT1 protein is associated with longevity.

“Moreover, we found that promotion of the NAD+-dependent SIRT1 mediated deacetylase activity, a key regulator in calorie restriction extension of life span, may be a mechanism by which calorie restriction influences AD-type brain amyloidosis in squirrel monkeys (Saimiri Sciureus),” says the study.

Control group lived longer
However, it is worth noting that although the calorie restricted group showed higher levels of the SIRT1 protein, the control group actually lived longer. The monkeys in the full-calorie control group lived to between 20 to 27 years of age – dying from congestive heart failure, liver failure or complication of intestinal bleeding. While the calorie restricted group lived from 15 to 20 years before succumbing to inanition, complications of bleeding or complications from liver necrosis.

Still, other health factors aside, the study strengthens the possibility that calorie restriction may exert beneficial effects in delaying the onset of AD.

There are no known cures or effective preventive strategies for the disease. Genetics play a role in early-onset cases, but appear to have less influence in the most common form of Alzheimer’s, late-onset-sporadic cases. - (Decision News Media, September 2006)


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