Sydney, Australia (PRWEB) June 21, 2013
In an article on Science Daily's website, there has been evidence showing that restricting caloric intake can activate an enzyme called Sirtuin 1, or SIRT1, which may offer protection against age-associated impairments in the brain. In light of this information, it could mean not only benefits of slowing the progression of age related brain impairments, but also with reducing the weight of individuals who are overweight, ultimately extending their lifespan.
In the study, Li-Huei Tsai PhD, Johannes Graf, PhD, and others at the Picower Institute For Learning and Memory, Massachusetts Institute of Technology, and Howard Hughes Medical Institute of Technology, and Howard Hughes Medical Institute, have been investigating whether reducing the amount of calories ingested into the body would delay the onset of nerve cell damage that is common with neurodegenerative diseases. If so, the team is investigating if the activation of SIRT1 was helping to drive the effect. They found that not only has caloric restriction has been found to delay nerve cell loss, but has discovered that a drug that activates SIRT1 can produce the same effects.
Although not involved in this study, Luigi Puglielli, MD, PhD, who studies aging, said, "There has been great interest in finding compounds that mimic the benefits of caloric restriction that could be used to delay the onset of age-associated problems and/or diseases."
He went on to add, "If proven safe for humans, this study suggests such a drug could be used as a preventive tool to delay the onset of neurodegeneration associated with several diseases that affect the aging brain."
Tsai’s team decreased the normal diets of genetically engineered mice by 30 percent. These mice were engineered to rapidly undergo changes in the brain associated with neurodegeneration. After three months of study on the mice, it was found that they completed several learning and memory tests. "We not only observed a delay in the onset of neurodegeneration in the calorie-restricted mice, but the animals were spared the learning and memory deficits of mice that did not consume reduced-calorie diets," Tsai concluded.
After the initial test, another study began on a different set of mice, where diet wasn’t changed, but the introduction of a drug that activated SIRT1 was introduced. Similarly to the first set of mice, the new set of mice had less cell loss and better cellular connectivity than mice that didn’t receive the drug.
"The question now is whether this type of treatment will work in other animal models, whether it's safe for use over time, and whether it only temporarily slows down the progression of neurodegeneration or stops it altogether," Tsai said.
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