Fight Aging!

In the course of exploring mammalian biochemistry, researchers are turning up ways to somewhat enhance the performance and slow the progressive decline of the brain. If pushed through to human therapies, this would all be a matter of poor patches over damage - not addressing the underlying issues at all, which means the performance will be poor and the costs of development still high. But working towards slowing down aging and patching over the end consequences rather than addressing their roots is unfortunately the focus of modern medical science. It's just one of the many things that must change if we are to see significant progress towards engineered human longevity in our lifetimes.

So that said, here are a couple of items for you to look at today relating to ongoing research into the mechanisms of the brain. The first involved CREB1, which if you look back in the archives you'll see is associated with memory and important in calorie restriction - and here researchers are confirming its lynch-pin status in the mechanisms by which calorie restriction produces benefits, in the brain at least:

Eating less keeps the brain young:

A team of Italian researchers at the Catholic University of Sacred Heart in Rome have discovered that this molecule, called CREB1, is triggered by "caloric restriction" (low caloric diet) in the brain of mice. They found that CREB1 activates many genes linked to longevity and to the proper functioning of the brain. ... Many studies suggest that obesity is bad for our brain, slows it down, causes early brain aging, making it susceptible to diseases typical of older people as the Alzheimer's and Parkinson's. In contrast, caloric restriction keeps the brain young. Nevertheless, the precise molecular mechanism behind the positive effects of an hypocaloric diet on the brain remained unknown till now.

The Italian team discovered that CREB1 is the molecule activated by caloric restriction and that it mediates the beneficial effects of the diet on the brain by turning on another group of molecules linked to longevity, the "sirtuins". This finding is consistent with the fact that CREB1 is known to regulate important brain functions as memory, learning and anxiety control, and its activity is reduced or physiologically compromised by aging. Moreover, Italian researchers have discovered that the action of CREB1 can be dramatically increased by simply reducing caloric intake, and have shown that CREB is absolutely essential to make caloric restriction work on the brain. In fact, if mice lack CREB1 the benefits of caloric restriction on the brain (improving memory, etc.) disappear.

The second item touches on an new way of improving memory function in mice. You'll note that this is one of many uncovered in recent years, and there has been quite the boom in finding ways to improve the memory of mammals, and even restore the capacity for memory in old animals.

Neuroscientists boost memory using genetics and a new memory-enhancing drug:

The authors discovered that mice lacking PKR in the brain have a kind of "super" memory. "We found that when we genetically inhibit PKR, we increased the excitability of brain cells and enhanced learning and memory, in a variety of behavioral tests," he said. For instance, when the authors assessed spatial memory (the memory for people, places and events) through a test in which mice use visual cues for finding a hidden platform in a circular pool, they found that normal mice had to repeat the task multiple times over many days in order to remember the platform's location. By contrast, mice lacking PKR learned the task after only one training session.

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Another key finding made by Costa-Mattioli and his team of researchers was the fact that this process could be mimicked by a PKR inhibitor - a small molecule that blocks PKR activity and thus acts as a "memory-enhancing drug."

"It is indeed quite amazing that we can also enhance both memory and brain activity with a drug that specifically targets PKR". Definitely then, the next step is to use what we have learned in mice and to try to improve brain function in people suffering from memory loss, said Costa-Mattioli.