French post-Impressionist artist Paul Gauguin famously once said, “I shut my eyes in order to see,” meaning he shut out the rest of the world to come up with great ideas.

More than a century later, scientists are able to prove Gauguin was onto something.

In the 1990s, cognitive scientists John Kounios and Mark Beeman started studying the insightful moment when you’re suddenly able to see things differently, also known as the “aha!” or eureka moment.

This moment occurs when you go from being stuck on a problem to having the ability to reinterpret a “stimulus, situation, or event to produce a nonobvious, nondominant interpretation.”

Through their extensive research, Kounios, a professor of psychology at Drexel University, and Beeman, of Northwestern, found that milliseconds before epiphanies, the activity in the brain’s visual area basically shuts down. That’s the moment right before the solution hits you. Kounios calls this moment a “brain blink,” which is when your brain turns inward just before the “aha!”

A simple example to illustrate this, Kounios tells Fast Company, is when you ask someone a tough question and they look away or down so they can think of the solution. In that moment, their brain is momentarily reducing visual input.

In the lab, Kounios and Beeman, authors of the upcoming book The Eureka Factor, used puzzles and problems to study brain activity. They found that right before the problem is presented, activity in the visual part of an analytical person’s brain would amp up to take in as much information as possible. On the other hand, the visual cortex would shut down for those who don’t solve problems in a methodical way, which allows them to block out the environment, look inward, and “find and retrieve subconscious ideas,” says Kounios.

THE VISUAL PARADOX

While more creative people shut down visual information before their “aha!” moment, these people tend to take in more visuals compared to others on a daily basis. Kounios says when these people walk down the street, they tend to study others, take in information, and may seem very scattered about their own agenda. However, the information they take in and synthesis may be a product of unconscious processing for years before ideas emerge. Those who are more analytical are more focused with their attention. When they walk down the street, they are focused on where they’re going and how they’re going to get there. They tend not to stray into different areas of thoughts.

Research on the “aha!” moment began more than a century ago, but it wasn’t until neuroimaging, which shows where cognitive change is happening, and electrophysiological techniques, which shows when cognitive change is happening, were scientists able to see what happens when the brain goes from a state where there’s no idea to a flow of creative insights.

Before brain imaging was readily available, researchers believed that the mental process was a gradual change, says Kounios. Your brain is always working, acquiring information that you can brew or incubate for years, but the change right before all that information pops into awareness isn’t gradual. It’s a burst of activity that can happen at any time and there’s nothing that you can do to force or coax it, he explains.

THE ROLE OF SLEEP AND MOOD

What you can do is be receptive and expose yourself to a lot of insight triggers. Also, positive moods tend to promote eureka moments. On the contrary, anxiety will promote analytical thoughts.

Lastly, Kounios advises to people who want epiphanies to get more sleep.

“There’s a process of memory consolidation that happens when you sleep,” he says. “These memories are transformed … they bring out hidden details or non-obvious connections between ideas. Getting lots of sleep leads to insights.”

If all else fails, simply follow Gauguin’s process and look inward instead of outward to come up with your next best ideas.

Scientists have raised hopes that brain damage caused by strokes, stab wounds and even bullets could one day be repaired by converting structural cells into functioning neurons.

For the first time, they have managed to regenerate damaged areas of the cerebral cortex of living animals by transforming a type of support cell found in the brain.

The cerebral cortex, which is the outer layer of tissue in the brain, is involved in controlling movement, interpreting the senses, conscious thought and memory. Usually almost no new neurons are grown in this area of the brain in adults, so once the cells are damaged or die, they are not replaced.

However, by injecting mice with viruses carrying a short piece of extra genetic code, scientists were able to coax structural cells, called NG2 glia, in the damaged part of the brain to develop into neurons. These then grew in the injured area and were found to be capable of receiving signals from neurons around the damaged area.

The study raises hopes that damaged brain tissue can be repaired in patients who suffer from epilepsy, or those who have had a stroke or a traumatic injury.

Scientists have previously used stem cells grown in the laboratory, which were then injected into patients, to help repair damage caused by stroke.

However, the latest research, which is published in the journal Stem Cell Reports, raises the prospect of repairing injuries using cells that are already in the patient’s head, reducing the risk of rejection and other complications.

The researchers cautioned, however, that it could take up to two decades before such therapies are ready to be used in human patients.

Dr Benedikt Berninger, a geneticist at the Ludwig-Maximillians University in Munich who was one of the lead researchers, said: “A lot of basic research is required until the field can move to clinics.”

“In the cortex we can think of Alzheimer’s disease and stroke, but these diseases involve massive tissue degeneration, so it will be difficult. Other diseases like epilepsy may be more amenable,” he added. “Regenerating neurons that relay sensory or motor responses is certainly more likely to work than regenerating memory circuits.”

Creating new neurons will not restore memories that were coded in the connections between degenerating cells, he said, but it may at least allow the system to acquire new memories.

The scientists genetically modified retroviruses to carry genes for the transcription factor Sox2, which is known to play an important role in the development of stem cells. The team injected the viruses into the damaged brains of mice, where they incorporated the genetic information into cells.

This transformed adult NG2 glia cells (which normally help maintain the physical structure of the brain and supply it with nutrients) into neurons. The new neurons only grew in the injured areas and did not grow in the brains of uninjured mice.

By measuring the electrical conductance of the new cells, the scientists were able to confirm that the new neurons had been incorporated into the brain’s neural networks and could receive signals.

Prof Magdalena Götz, a neuroscientist at Ludwig-Maximilians University Munich who was involved in the research, said that they hoped to develop drugs to promote the transformation of the cells rather than using viruses.

“We have to cope with the neurons we are born with for the rest of our life in most brain regions. Once we lose a certain number, there is presently nothing one can do to make new neurons,” she said. “Therefore it is so important to study how cells in the brain could be inspired to generate new neurons when needed.”

Professor Anthony Hollander, head of the Institute of Integrative Biology at the University of Liverpool, described the latest work as encouraging. “The most interesting observation here is that injured brain tissue appears to be a better environment for this to happen than normal brain tissue, which is obviously a good thing if the aim ultimately is to treat injured tissue,” he said.

“It is far too early to say if this observation will be of clinical relevance – for example the nature of injury could be critical and the time after injury could be equally important.”

Seals brought tuberculosis to South America long before Columbus sailed to the New World, a new study shows.

An analysis of tuberculosis DNA recovered from three 700- to 1,000-year-old Peruvian skeletons reveals that the strain of TB in the ancient bones doesn’t match the strain brought to the New World by European explorers. Instead, it closely resembles one that infects seals in the Southern Hemisphere, an international group of researchers reports August 20 in Nature.

Researchers had long thought that Mycobacterium tuberculosis, the bacterium that causes TB, originated in cattle as M. bovis, jumped to humans after dairy cows were domesticated and then came to the Americas with Europeans.

Scientists have long been searching for the factor that determines why humans often behave so selflessly. It was known that humans share this tendency with species of small Latin American primates of the family Callitrichidae (tamarins and marmosets), leading some to suggest that cooperative care for the young, which is ubiquitous in this family, was responsible for spontaneous helping behavior. But it was not so clear what other primate species do in this regard, because most studies were not comparable.

Stephen Hawking turns 70 on Sunday, beating the odds of a daunting diagnosis by nearly half a century.

The famous theoretical physicist has helped to bring his ideas about black holes and quantum gravity to a broad public audience. For much of his time in the public eye, though, he has been confined to a wheelchair by a form of the motor-neuron disease amyotrophic lateral sclerosis (ALS). And since 1985 he has had to speak through his trademark computer system—which he operates with his cheek—and have around-the-clock care.

But his disease seems hardly to have slowed him down. Hawking spent 30 years as a full professor of mathematics at the University of Cambridge. And he is currently the director of research at the school’s Center for Theoretical Cosmology.

But like his mind, Hawking’s illness seems to be singular. Most patients with ALS—also known as Lou Gehrig’s disease, for the famous baseball player who succumbed to the disease—are diagnosed after the age of 50 and die within five years of their diagnosis. Hawking’s condition was first diagnosed when he was 21, and he was not expected to see his 25th birthday.

Why has Hawking lived so long with this malady when so many other people die so soon after diagnosis? We spoke with Leo McCluskey, an associate professor of neurology and medical director of the ALS Center at the University of Pennsylvania, to find out more about the disease and why it has spared Hawking and his amazing brain.

[An edited transcript of the interview follows.]

What is ALS—and is there more than one form of it?
ALS, which is also known as a motor-neuron disease—and colloquially as Lou Gehrig’s disease in the U.S.—is a neurodegenerative disease. Each muscle is controlled by motor neurons that reside in the brain in the frontal lobe. These are controlled electrically and are synaptically connected to motor neurons that reside lower down in the brain—as well as motor neurons that reside in the spinal cord. The guys in the brain are called the upper motor neurons, and the guys in the spine are called the lower motor neurons. The disease causes weakness of either upper motor neurons or lower motor neurons or both.

It’s been known for quite some time that there are variants of ALS. One is referred to as progressive muscular atrophy, or PMA. It appears to be an isolated illness of the lower motor neurons. However, pathologically, if you do an autopsy of a patient, they will have evidence of deterioration of upper motor neurons.

There is also primary lateral sclerosis—PLS—and clinically it looks like an isolated upper motor-neuron disorder. However, pathologically they also have lower motor-neuron disorder.

The other classic syndrome is called progressive baldor palsy—or progressive supranuclear palsy—which is weakening of cranial muscles, like the tongue, face and swallowing muscles. But it pretty much always spreads to limb muscles.

Those are the four classic motor-neuron disorders that have been described. And it was thought for quite some time that these disorders were limited to motor neurons. It’s now clear that that’s not true. It’s now well recognized that 10 percent of these patients can develop degeneration in another part of the brain, such as other parts of the frontal lobe that don’t contain the motor neurons or the temporal lobe. So some ofthese patients can actually develop dementia, called frontal-temporal lobe dementia.

One of the misconceptions about ALS is that it’s only a motor-neuron disease, and that’s not true.

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