Bad drivers may in part have their genes to blame, suggests a new study by UC Irvine neuroscientists.

People with a particular gene variant performed more than 20 percent worse on a driving test than people without it – and a follow-up test a few days later yielded similar results. About 30 percent of Americans have the variant.

“These people make more errors from the get-go, and they forget more of what they learned after time away,” says Dr. Steven Cramer, neurology associate professor and senior author of the study published recently in the journal Cerebral Cortex.

This gene variant limits the availability of a protein called brain-derived neurotrophic factor during activity. BDNF keeps memory strong by supporting communication among brain cells and keeping them functioning optimally. When a person is engaged in a particular task, BDNF is secreted in the brain area connected with that activity to help the body respond.

Previous studies have shown that in people with the variant, a smaller portion of the brain is stimulated when doing a task than in those with a normal BDNF gene. People with the variant also don’t recover as well after a stroke. Given these differences, the UCI scientists wondered: Could the variant affect an activity such as driving?

“We wanted to study motor behavior, something more complex than finger-tapping,” says Stephanie McHughen, graduate student and lead author of the study. “Driving seemed like a good choice because it has a learning curve and it’s something most people know how to do.”

The driving test was taken by 29 people – 22 without the gene variant and seven with it. They were asked to drive 15 laps on a simulator that required them to learn the nuances of a track programmed to have difficult curves and turns. Researchers recorded how well they stayed on the course over time. Four days later, the test was repeated.

Results showed that people with the variant did worse on both tests than the other participants, and they remembered less the second time. “Behavior derives from dozens and dozens of neurophysiologic events, so it’s somewhat surprising this exercise bore fruit,” Cramer says.

The gene variant isn’t always bad, though. Studies have found that people with it maintain their usual mental sharpness longer than those without it when neurodegenerative diseases such as Parkinson’s, Huntington’s and multiple sclerosis are present.

“It’s as if nature is trying to determine the best approach,” Cramer says. “If you want to learn a new skill or have had a stroke and need to regenerate brain cells, there’s evidence that having the variant is not good. But if you’ve got a disease that affects cognitive function, there’s evidence it can act in your favor. The variant brings a different balance between flexibility and stability.”

A test to determine whether someone has the gene variant is not commercially available.

“I’d be curious to know the genetics of people who get into car crashes,” Cramer says. “I wonder if the accident rate is higher for drivers with the variant.”

In addition to Cramer and McHughen, Paul Rodriguez, Laura Marchal-Crespo and Vincent Procaccio of UCI worked on the study, along with researchers from the University of Florida. The National Institutes of Health funded the study.

Nine research teams from universities across the U.S. will study how interactive video games such as the Wii Active could help fight childhood obesity and how mobile phone games could help smokers quit or reduce tobacco use.

The teams will also focus on how video games can be designed to help people change behaviors and self-manage chronic illnesses as well as improve communication with autistic patients.

“Digital games are interactive and experiential, and so they can engage people in powerful ways to enhance learning and [change health-related behavior], especially when they are designed on the basis of well-researched strategies,” said Debra Lieberman, a communication researcher at the University of California, Santa Barbara, Institute for Social, Behavioral, and Economic Research.

Lieberman, a leading expert in the research and design of interactive media for learning and health behavior change, said the new interactive gaming studies will provide “cutting-edge, evidence-based strategies that designers will be able to use in the future to make their health games more effective.”

The nine teams, chosen from among 185 proposals, have been awarded between $100,000 and $300,000 each from $1.85 million in grant money offered by the Robert Wood Johnson Foundation.

The researchers will lead one- to two-year studies of digital games that engage players in physical activity and/or motivate them to improve how they take care of themselves through healthy changes in lifestyle, prevention behaviors, cognitive, social or physical skills, chronic disease self-management, and/or adherence to a medical treatment plan.

For example, the research teams will delve into the popular dance pad video game Dance Revolution to see how it might help Parkinson’s patients reduce the risk of falling, or how facial recognition games might be designed to help people with autism better identify others’ emotions.

The studies will focus on diverse population groups that vary by race and ethnicity, health status, income level and game-play setting, with age groups ranging from elementary school children to 80-year-olds. The research teams will study participants’ responses to health games played on a variety of platforms, such as video game consoles, computers, mobile phones and robots.

“The pace of growth and innovation in digital games is incredible, and we see tremendous potential to design them to help people stay healthy or manage chronic conditions like diabetes or Parkinson’s disease. However, we need to know more about what works and what does not, and why,” Paul Tarini, team director for the Robert Wood Johnson Foundation’s Pioneer Portfolio, said in a statement.

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By Laura Sanders, Science News

CHICAGO — A toned, buff bod isn’t the only thing a workout is good for. Exercise protects special brain cells in monkeys’ brains and improves motor function, a new study finds. The data, presented at a news briefing October 18 in Chicago at the Society for Neuroscience’s annual meeting, adds to a growing body of evidence that shows exercise is good for the brain, too.

“This is sort of a quiet revolution that’s been occurring in neuroscience,” says Carl Cotman, a brain aging expert at the University of California, Irvine, “to realize that physical activity at a certain level impacts the brain in a really profound way.”

In the new study, researchers led by Judy Cameron of the University of Pittsburgh trained six adult female rhesus monkeys to run on treadmills built for humans. Over a period of three months, monkeys either ran, jogged or sat on a treadmill for five hours each week. Monkeys that ran got their heart rates to about 80 percent of maximum, comparable to a human training program that would increase cardiovascular fitness. The jogging monkeys’ heart rates reached about 60 percent of maximum.

After this training period, the researchers hit the right side of the monkeys’ brains with a neurotoxin called MPTP, designed to selectively kill neurons that produce the signaling chemical dopamine. These neurons, and the dopamine they produce, regulate movement, and are the very same ones that die in people with Parkinson’s disease.

Sedentary monkeys showed the expected decrease in these dopamine neurons on the right side of the brain after the neurotoxin was applied. But in the brains of monkeys that had run for the past three months, the neurotoxin had almost no effect. In the runners, dopamine neurons were just as plentiful on the right side of the brain as on the left.

Jogging also had a protective effect, although slightly weaker than running’s, Cameron says. “This is really good news. It means that any little bit more activity you can do is positive for your brain,” says Cameron. “Your brain seems very sensitive to exercise.”

When the researchers continued the experiment for another six weeks, the results held. A brain scan revealed that “the animals that were exercising had virtually no loss of dopamine in those neurons,” Cameron says. “We think that exercise is very neuroprotective.”

Next, the researchers assessed the monkeys’ ability to use the hand affected by the neurotoxin. Monkeys had to retrieve a Lifesaver candy from a thin wire, an experiment designed to test motor coordination. Sedentary monkeys could not use their left, affected hand at all, while the runners showed no difference between their left and right hands, the researchers found.

The new study highlights the importance of exercise for maintaining a healthy brain. Other studies presented at the meeting have found that exercise has a wide range of brain-protective roles in mice, monkeys and humans.

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Your brain excels when you give it good nourishment, physical exercise, keep the stress down, get the right amount of sleep, and push it novel directions like using Myfitbrain.

A research team from the University of California, San Diego School of Medicine and the Salk Institute for Biological Studies in La Jolla has identified a protein in the brain of mice that protects neurons from excessive inflammation, which can lead to neurodegenerative disorders such as Parkinson’s disease. Their study, which identifies the protective function of a protein called Nurr1 and defines the pathway by which it works, will be published in the April 3 edition of the journal Cell.

Nurr1 is a transcription factor that has been known for some time to play an essential role in the generation and maintenance of dopaminergic neurons in the brain. Rare mutations in Nurr1 are associated with familial Parkinson’s disease, and the loss of dopaminergic neurons — which are the main source of dopamine in the central nervous system — is associated with the disease. Dopamine helps control multiple brain functions such as movement, attention, pleasure, emotion and motivation. The new findings have uncovered a second and previously unexpected role of the Nurr1 protein in two other cell types in the brain — microglia and astrocytes. The brain’s microglia are macrophage-like cells that are active components of the immune defense in the central nervous system, while astrocytes are large star-shaped cells that normally play important support functions in the brain.
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BUFFALO, N.Y. — University at Buffalo researchers have identified a new mechanism that plays a central role in adult brain stem cell development and prompts brain stem cells to differentiate into neurons.

Their discovery, known as Integrative FGFR1 Signaling (INFS), has fundamentally challenged the prevailing ideas of how signals are processed in cells during neuronal development.

The INFS mechanism is considered capable of repopulating degenerated brain areas, raising possibilities for new treatments for Parkinson’s disease, Alzheimer’s disease and other neurodegenerative disorders, and may be a promising anti-cancer therapy.

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