A new study finds that limiting food intake can activate genes linked to longevity and brain function, which could lead to new treatments to extend life, improve memory and reduce risk of dementia.

The researchers found that consuming fewer calories triggered a protein known as CREB1, which activates genes known to prolong life and improve brain function. This finding supports previous studies that obesity causes early brain aging, making it susceptible to diseases typical of older people, such as the Alzheimer's and Parkinson's.

Many studies have shown that animals given just 70 percent of the calories they of their normal diet lived a one-third longer than average, at the same time demonstrated better memory and mental function.

Various studies have also shown that caloric-restricted mice did not become obese, develop diabetes or Alzheimer's disease, and showed greater cognitive performance and memory.

But the precise molecular mechanism that triggered the positive effects of a calorie-restricted diet on the brain was unknown until this recent study.

The Italian research team discovered that CREB1 is activated by caloric restriction, which in turn triggers the activation the "sirtuins," another group of molecules linked to longevity.

"Our findings identify for the first time an important mediator of the effects of diet on the brain," said lead researcher Dr. Giovambattista Pani at the Institute of General Pathology, Faculty of Medicine at the Catholic University of Sacred Heart in Rome.

The new finding is consistent with the fact that CREB1 is known to regulate important brain functions such as memory, learning and anxiety control, and its activity is reduced or physiologically compromised by aging.

The action of CREB1 can be dramatically increased by simply reducing caloric intake, according to the study, and showing that CREB is absolutely essential to make caloric restriction work on the brain. Specifically, the experimental mice which lacked CREB1 showed the same brain disabilities typical of overfed or older animals.

"This discovery has important implications to develop future therapies to keep our brain young and prevent brain degeneration and the aging process. In addition, our study shed light on the correlation among metabolic diseases as diabetes and obesity and the decline in cognitive activities," Dr. Pani said.

"Our hope is to find a way to activate CREB1, for example through new drugs, so to keep the brain young without the need of a strict diet," said Dr. Pani in their study which appeared week in the Proceedings of the National Academy of Sciences USA.