Eating less may keep the mind young

Eating less may keep the mind young, according to Italian scientists who reported Monday they have discovered the molecular process by which a strict diet may save the brain from the ravages of age.

  Strict diet could save brain from aging: study

The research, published in the US journal the Proceedings of the National Academy of Sciences, is based on a study of mice that were fed a diet of about 70 percent of the food they normally consumed. 

Scientists found the calorie-restricted diet triggered a protein molecule, CREB1, that activates a host of genes linked to longevity and good brain function.

"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 lead author Giovambattista Pani, researcher at the Institute of General Pathology, Faculty of Medicine at the Catholic University of Sacred Heart in Rome.

Researchers have previously discovered that mice on diets showed better cognitive abilities and memory, less aggression, and tended to avoid or delay Alzheimer's disease. But they have not known exactly why."CREB1 is known to regulate important brain functions as memory, learning and anxiety control, and its activity is reduced or physiologically compromised by aging," said the study.

Mice that were genetically altered to lack CREB1 showed none of the same memory benefits if they were on a low-calorie diet as mice that had the molecule, and showed the same brain disabilities as mice that were overfed.

"Thus, our findings identify for the first time an important mediator of the effects of diet on the brain," Pani said."This discovery has important implications to develop future therapies to keep our brain young and prevent brain degeneration and the aging process."

According to Marc Gordon, chief of neurology at Zucker Hillside Hospital in Glen Oaks, New York, the findings could shed new light on why some people who are obese in middle age encounter cognitive problems later in life."Mid-life obesity has been associated with late-life dementia. However, the physiological basis for this association remains unclear," said Gordon, who was not part of the study.

"These investigators have studied the effects of limiting caloric intake in mice, and have identified a biochemical pathway that may mediate at least some of the brain's responses to dietary restriction."

“Super memory” pill–and possibly an Alzheimer’s cure–could be around the corner!

By Eric Pfeiffer | The Sideshow

Scientists have isolated a gene in mice that works to give them "super memories" and reverses the course of several degenerative mental illnesses like Alzheimer's. And because of the similarity of mice and human brains, a powerful brain pill for humans may now not be far off.

The brains of both mice and humans release a gene known as PKR, which is triggered by the onset of Alzheimer's. But the newly discovered gene can apparently block PKR's release--a development that not only can reverse the course of degenerative brain diseases such as Alzheimer's, but induces a state of "super memory" in the mice it has been tested on.

"If we were to find an inhibitor, a molecule, a drug that will specifically block PKR, we should be able to do the same [in humans]," Maura Costa-Mattioli, who led the research study at Baylor University, told the Vancouver Sun. "And we did."

"We recognize that PKR plays a dual role, one in regulating simple everyday processes like the way neurons talk to each other [for] memory, but also has a stress response," added John Bell, a senior scientist at the Ottawa Hospital Research Institute who also contributed to the study.

More from the Sun:

A virus is one form of stress that triggers PKR, but Alzheimer's patients' brains also experience PKR-releasing stress, said Bell, whose cancer research led him to create PKR-deficient mice which he shared with Costa-Mattioli's lab. Researchers found that when PKR is genetically suppressed in mice, another immune molecule, called gamma interferon, increases communication between neurons, improving memory and making brain function more efficient, Costa-Mattioli said.

Reportedly, when PKR is blocked, the gamma interferon can work more or less spontaneously to improve brain functions--and can be activated via a simple PKR-inhibitor injection into a mouse's stomach rather than through more conventional and drawn-out gene therapy. The possible application for humans would lead to something like taking a "brain pill" to treat diseases like Alzheimer's, or simply to give the memory a significant boost:

When the researchers tested the PKR-deficient mice in a series of memory tests, those mice were able to pick up on patterns and remember them on the first try, while the other mice needed days to figure out how to solve the puzzle. The PKR-deficient mice consistently showed significantly better memory and learning abilities than their counterparts.

Of course, Costa-Mattioli said the goal is not to create a new society of super-memory powered people.

"Let's say we'd compare with Viagra. People use Viagra at whatever age, let's say 60, 65. But someone (who) is 40 goes to buy it, they can get it," he said. "But this is not our goal . . . Our goal would be to treat people who have a memory problem."