The red sheath around these neurons may stop their growth. / Image courtesy Takao Hensch
Vancouver, British Columbia—Infancy is filled with the best of times: critical windows of weeks and months when the growing brain fine-tunes things like language skills and vision. And it’s wise to take advantage of them, for when the windows slam shut, those skills don’t develop. Or so scientists used to think.
Upsetting conventional wisdom, several scientists came here to the annual meeting of the American Association for the Advancement of Science to show how those windows actually can be moved earlier or later in infant development. Drug and behavioral interventions can prop them open. And moving them later seems to give children who missed the windows because of illness a second chance to develop those skills—in one case, even giving adults who had been blind at birth a chance to recover their eyesight.
“We are talking about making old brains young again,” said Takao Hensch, a professor of neurology at Harvard Medical School whose work with rats has focused on molecules and chemicals in the brain that help to open and close the windows. “Perhaps we can restore a juvenile brain state, temporarily, if we wanted to recover lost function in a brain region after a stroke.”
Yet he and others worry that restoring periods of brain growth could have serious risks. Mental illnesses like schizophrenia have been linked to unbridled growth. “There’s an ethical question we have to deal with: Just because we can do it, should we?” Mr. Hensch asked.
The critical windows exist because the brain is “plastic”—it rewires itself, forming new connections between neurons, in response to stimulation from the environment. The connections enable the acquisition of new skills. Normally that plasticity peaks in the first several months of life, but at different times for different skills. For instance, the ability to pick out one’s native language from the babble of sounds in the world—paying more attention to it than to words in another tongue—normally peaks at about six months and then winds down, said Janet Werker, a professor of psychology at the University of British Columbia, in Vancouver.
But that timing changes in babies born to mothers suffering from depression, she said. Tests show those kids peak later, at about 10 months. There’s an opposite effect in infants with depressed mothers who are taking Prozac-like antidepressants, known as serotonin-reuptake inhibitors. Their peaks move forward by a few months. Ms. Werker emphasized that the differences are subtle and show up on fine-grained psychological tests.
“At this point we don’t know if acceleration or delay leads to any language deficits later in life,” she said. But the periods might move back in infants of depressed mothers because such mothers talk less and play less with their babies. And mothers taking antidepressants during pregnancy may pass enough of the medication to fetuses to stimulate and accelerate this learning window.
Mr. Hensch, in experiments with rats, has identified a number of molecules that become what he calls “brakes” on the brain’s ability to grow new connections. Many of the molecules reside in myelin, a fatty sheath around pathways between neurons. “As myelin becomes more leaky, though, growth increases,” he said. Another brake is a plastic-wrap-like membrane that surrounds neurons, called a peri-neuronal sheath. Rats raised in total darkness usually—and not surprisingly—have abnormal vision and lose the ability to focus on details. But using enzymes to peel back the peri-neuronal sheath rescues them from that deficit, he said.
Playing a video game called Medal of Honor helped some people recover lost visual abilities.
People raised with obstructed vision also suffer from deficits. Children born with congenital cataracts never have completely normal eyesight even after the cataracts are removed surgically and replaced by contact lenses, said Daphne Maurer, a professor of psychology at McMaster University, in Hamilton, Ontario. “They don’t attend to detail, or follow motion as well as normal children,” she said. Babies begin learning to see at birth, she said, and the window for vision improvement appears to shut around age 7.
In some adults who had cataracts as infants, however, she was able to reopen it. And she used intense behavioral stimulation to do it. She had six of those people play a “first-person shooter” video game called Medal of Honor. They played for 40 hours, spread over a four-week period. “The game forces you to pay attention to a moving focus of action, and different details at different points on the screen,” she said.
Five of the six adults showed slight but definite improvement. They were better at reading small print and following the direction of moving dots in vision tests. “It’s like seeing two lines better on the eye chart,” Ms. Maurer said. But not everything got better: Binocular vision—using both eyes together—did not improve, indicating visual development, and repair, is not a uniform process. (Ms. Maurer and some colleagues are now developing their own less-violent video game to experiment with in therapy. “I didn’t relish asking people to play a ‘first-person shooter’ for 40 hours,” she said.)
It’s unclear how video games might be rewiring the brain. Mr. Hensch said that one of the brake molecules he studies, called Lynx1, inhibits the neurotransmitter acetylcholine. And other research has shown that acetylcholine is released when a person is aroused and excited, like when they are playing a video game. It’s possible, he said, that arousal “breaks through the brakes.”
Taking off the brakes on brain development may have a downside, however. During the natural critical windows, the brain is “tuning itself” to its environment, said Ms. Maurer. Extending the period could throw off the balance of learning in some yet-unknown way, she said.
Mr. Hensch added that “nature has provided the brakes for a reason. In postmortem studies of people with mental illness, we see brains with impaired brakes.” Brains of people with schizophrenia, for instance, or bipolar disorder, show overgrowth of neuronal connections in some areas, compared with brains of people without those diseases. There is no known cause-and-effect relationship, but there is some speculation that normal learning and stimulation pathways get thrown off. “So opening up these brakes, before we understand exactly what they do, could be dangerous,” Mr. Hensch said.
