New research may help explain why curiosity promotes better memory

Everyone knows it’s easier to learn about a topic you’re curious about. Now, a new study reveals what’s going on in the brain during that process, revealing that such curiosity may give a person a memory boost.

When participants in the study were feeling curious, they were better at remembering information even about unrelated topics, and brain scans showed activity in areas linked to reward and memory.

The results, detailed October 2 in the journal Neuron, hint at ways to improve learning and memory in both healthy people and those with neurological disorders, the researchers said.

“Curiosity may put the brain in a state that allows it to learn and retain any kind of information, like a vortex that sucks in what you are motivated to learn, and also everything around it,” Matthias Gruber, a memory researcher at the University of California, Davis, said in a statement. “These findings suggest ways to enhance learning in the classroom and other settings.”

Gruber and his colleagues put people in a magnetic resonance imaging (MRI) scanner and showed them a series of trivia questions, asking them to rate their curiosity about the answers to those questions. Later, the participants were shown selected trivia questions, then a picture of a neutral face during a 14-second delay, followed by the answer. Afterward, the participants were given a surprise memory test of the faces, and then a memory test of the trivia answers.

Not surprisingly, the study researchers found that people remembered more information about the trivia when they were curious about the trivia answers. But unexpectedly, when the participants were curious, they were also better at remembering the faces, an entirely unrelated task. Participants who were curious were also more likley than others to remember both the trivia information and unrelated faces a day later, the researchers found.

The brain scans showed that, compared with when their curiosity wasn’t piqued, when people were curious, they showed more activation of brain circuits in the nucleus accumbens, an area involved in reward. These same circuits, mediated by the neurochemical messenger dopamine, are involved in forms of external motivation, such as food, sex or drug addiction.

Finally, being curious while learning seemed to produce a spike of activity in the hippocampus, an area involved in forming new memories, and strengthened the link between memory and reward brain circuits.

The study’s findings not only highlight the importance of curiosity for learning in healthy people, but could also give insight into neurological conditions. For example, as people age, their dopamine circuits tend to deteriorate, so understanding how curiosity affects these circuits could help scientists develop treatments for patients with memory disorders, the researchers said.

http://www.livescience.com/48121-curiosity-boosts-memory-learning.html

How Exercise Beefs Up the Brain

exercise

New research explains how abstract benefits of exercise—from reversing depression to fighting cognitive decline—might arise from a group of key molecules.

While our muscles pump iron, our cells pump out something else: molecules that help maintain a healthy brain. But scientists have struggled to account for the well-known mental benefits of exercise, from counteracting depression and aging to fighting Alzheimer’s and Parkinson’s disease. Now, a research team may have finally found a molecular link between a workout and a healthy brain.

Much exercise research focuses on the parts of our body that do the heavy lifting. Muscle cells ramp up production of a protein called FNDC5 during a workout. A fragment of this protein, known as irisin, gets lopped off and released into the bloodstream, where it drives the formation of brown fat cells, thought to protect against diseases such as diabetes and obesity. (White fat cells are traditionally the villains.)

While studying the effects of FNDC5 in muscles, cellular biologist Bruce Spiegelman of Harvard Medical School in Boston happened upon some startling results: Mice that did not produce a so-called co-activator of FNDC5 production, known as PGC-1α, were hyperactive and had tiny holes in certain parts of their brains. Other studies showed that FNDC5 and PGC-1α are present in the brain, not just the muscles, and that both might play a role in the development of neurons.

Spiegelman and his colleagues suspected that FNDC5 (and the irisin created from it) was responsible for exercise-induced benefits to the brain—in particular, increased levels of a crucial protein called brain-derived neurotrophic factor (BDNF), which is essential for maintaining healthy neurons and creating new ones. These functions are crucial to staving off neurological diseases, including Alzheimer’s and Parkinson’s. And the link between exercise and BDNF is widely accepted. “The phenomenon has been established over the course of, easily, the last decade,” says neuroscientist Barbara Hempstead of Weill Cornell Medical College in New York City, who was not involved in the new work. “It’s just, we didn’t understand the mechanism.”

To sort out that mechanism, Spiegelman and his colleagues performed a series of experiments in living mice and cultured mouse brain cells. First, they put mice on a 30-day endurance training regimen. They didn’t have to coerce their subjects, because running is part of a mouse’s natural foraging behavior. “It’s harder to get them to lift weights,” Spiegelman notes. The mice with access to a running wheel ran the equivalent of a 5K every night.

Aside from physical differences between wheel-trained mice and sedentary ones—“they just look a little bit more like a couch potato,” says co-author Christiane Wrann, also of Harvard Medical School, of the latter’s plumper figures—the groups also showed neurological differences. The runners had more FNDC5 in their hippocampus, an area of the brain responsible for learning and memory.

Using mouse brain cells developing in a dish, the group next showed that increasing the levels of the co-activator PGC-1α boosts FNDC5 production, which in turn drives BDNF genes to produce more of the vital neuron-forming BDNF protein. They report these results online today in Cell Metabolism. Spiegelman says it was surprising to find that the molecular process in neurons mirrors what happens in muscles as we exercise. “What was weird is the same pathway is induced in the brain,” he says, “and as you know, with exercise, the brain does not move.”

So how is the brain getting the signal to make BDNF? Some have theorized that neural activity during exercise (as we coordinate our body movements, for example) accounts for changes in the brain. But it’s also possible that factors outside the brain, like those proteins secreted from muscle cells, are the driving force. To test whether irisin created elsewhere in the body can still drive BDNF production in the brain, the group injected a virus into the mouse’s bloodstream that causes the liver to produce and secrete elevated levels of irisin. They saw the same effect as in exercise: increased BDNF levels in the hippocampus. This suggests that irisin could be capable of passing the blood-brain barrier, or that it regulates some other (unknown) molecule that crosses into the brain, Spiegelman says.

Hempstead calls the findings “very exciting,” and believes this research finally begins to explain how exercise relates to BDNF and other so-called neurotrophins that keep the brain healthy. “I think it answers the question that most of us have posed in our own heads for many years.”

The effect of liver-produced irisin on the brain is a “pretty cool and somewhat surprising finding,” says Pontus Boström, a diabetes researcher at the Karolinska Institute in Sweden. But Boström, who was among the first scientists to identify irisin in muscle tissue, says the work doesn’t answer a fundamental question: How much of exercise’s BDNF-promoting effects come from irisin reaching the brain from muscle cells via the bloodstream, and how much are from irisin created in the brain?

Though the authors point out that other important regulator proteins likely play a role in driving BDNF and other brain-nourishing factors, they are focusing on the benefits of irisin and hope to develop an injectable form of FNDC5 as a potential treatment for neurological diseases and to improve brain health with aging.

http://news.sciencemag.org/biology/2013/10/how-exercise-beefs-brain

Thanks to Dr. Rajadhyaksha for bringing this to the attention of the It’s Interesting community.

New research on adult neurogenesis shows that about 1,400 new brain cells are born every day, and about 80% of human brain cells in the dentate gyrus of the hippocampus undergo renewal in adulthood

ooold-neurons

bomb

by Leonie Welberg

The question of whether adult neurogenesis occurs in the human hippocampus has been a hotly debated topic in neuroscience. In a study published in Cell, Frisén and colleagues now settle the debate by providing evidence that around 1,400 dentate gyrus cells are born in the human brain every day.

The authors made use of a birth-dating method that is based on the principle that 14C in the atmosphere is taken up by plants and — because humans eat plants and animals that eat plants — eventually also by humans. As 14C is incorporated into DNA during cell division, the 14C content of a cell is thought to reflect 14C levels in the atmosphere at the time of the birth of the cell. Importantly, atomic bomb testing in the 1950s and 1960s resulted in a spike in atmospheric 14C levels, and levels declined after 1963; this means that the level of 14C in cellular DNA can be used as a relatively precise marker of a cell’s birth date.

The authors applied the 14C birth-dating method to whole hippocampi dissected from post-mortem brains donated by individuals who were born in different years in the twentieth century. They separated neurons from non-neuronal hippocampal cells, purified the neuronal DNA and determined 14C levels. Neuronal 14C levels did not match atmospheric 14C levels in the individual’s birth year but were either higher (for people born before 1950) or lower (for people born after 1963), suggesting that at least some of the hippocampal cells were born after the year in which an individual was born.

Computer modelling of the data revealed that the best-fit model was one in which 35% of hippocampal cells showed such turnover, whereas the majority did not (that is, they were born during development). Assuming that, in humans, adult neurogenesis would take place in the dentate gyrus rather than in other hippocampal areas (as it does in rodents), and as the dentate gyrus contains about 44% of all hippocampal neurons, this model suggests that about 80% of human dentate gyrus cells undergo renewal in adulthood. This is in striking contrast to the scenario in mice, in which only ~10% of adult dentate gyrus neurons undergo renewal. The study further showed that there is very little decline in the level of hippocampal neurogenesis with ageing in humans, which is again in contrast to rodents.

It is now well established that adult-born neurons have a functional role in the mouse and rat dentate gyrus and olfactory bulb. A previous study using the same neuronal birth-dating method established that no adult neurogenesis takes place in the olfactory bulb and cortex in humans, but the new study has elegantly shown that the situation is different in the dentate gyrus. Whether the adult-born neurons have functional implications in humans remains a topic for future investigation.

http://www.nature.com/nrn/journal/v14/n8/full/nrn3548.html?WT.ec_id=NRN-201308

Thanks to Kebmodee for bringing this to the attention of the It’s Interesting community.

Brain implants: Restoring memory with a microchip

130507101540-brain-implants-human-horizontal-gallery

William Gibson’s popular science fiction tale “Johnny Mnemonic” foresaw sensitive information being carried by microchips in the brain by 2021. A team of American neuroscientists could be making this fantasy world a reality. Their motivation is different but the outcome would be somewhat similar. Hailed as one of 2013’s top ten technological breakthroughs by MIT, the work by the University of Southern California, North Carolina’s Wake Forest University and other partners has actually spanned a decade.

But the U.S.-wide team now thinks that it will see a memory device being implanted in a small number of human volunteers within two years and available to patients in five to 10 years. They can’t quite contain their excitement. “I never thought I’d see this in my lifetime,” said Ted Berger, professor of biomedical engineering at the University of Southern California in Los Angeles. “I might not benefit from it myself but my kids will.”

Rob Hampson, associate professor of physiology and pharmacology at Wake Forest University, agrees. “We keep pushing forward, every time I put an estimate on it, it gets shorter and shorter.”

The scientists — who bring varied skills to the table, including mathematical modeling and psychiatry — believe they have cracked how long-term memories are made, stored and retrieved and how to replicate this process in brains that are damaged, particularly by stroke or localized injury.

Berger said they record a memory being made, in an undamaged area of the brain, then use that data to predict what a damaged area “downstream” should be doing. Electrodes are then used to stimulate the damaged area to replicate the action of the undamaged cells.

They concentrate on the hippocampus — part of the cerebral cortex which sits deep in the brain — where short-term memories become long-term ones. Berger has looked at how electrical signals travel through neurons there to form those long-term memories and has used his expertise in mathematical modeling to mimic these movements using electronics.

Hampson, whose university has done much of the animal studies, adds: “We support and reinforce the signal in the hippocampus but we are moving forward with the idea that if you can study enough of the inputs and outputs to replace the function of the hippocampus, you can bypass the hippocampus.”

The team’s experiments on rats and monkeys have shown that certain brain functions can be replaced with signals via electrodes. You would think that the work of then creating an implant for people and getting such a thing approved would be a Herculean task, but think again.

For 15 years, people have been having brain implants to provide deep brain stimulation to treat epilepsy and Parkinson’s disease — a reported 80,000 people have now had such devices placed in their brains. So many of the hurdles have already been overcome — particularly the “yuck factor” and the fear factor.

“It’s now commonly accepted that humans will have electrodes put in them — it’s done for epilepsy, deep brain stimulation, (that has made it) easier for investigative research, it’s much more acceptable now than five to 10 years ago,” Hampson says.

Much of the work that remains now is in shrinking down the electronics.

“Right now it’s not a device, it’s a fair amount of equipment,”Hampson says. “We’re probably looking at devices in the five to 10 year range for human patients.”

The ultimate goal in memory research would be to treat Alzheimer’s Disease but unlike in stroke or localized brain injury, Alzheimer’s tends to affect many parts of the brain, especially in its later stages, making these implants a less likely option any time soon.

Berger foresees a future, however, where drugs and implants could be used together to treat early dementia. Drugs could be used to enhance the action of cells that surround the most damaged areas, and the team’s memory implant could be used to replace a lot of the lost cells in the center of the damaged area. “I think the best strategy is going to involve both drugs and devices,” he says.

Unfortunately, the team found that its method can’t help patients with advanced dementia.

“When looking at a patient with mild memory loss, there’s probably enough residual signal to work with, but not when there’s significant memory loss,” Hampson said.

Constantine Lyketsos, professor of psychiatry and behavioral sciences at John Hopkins Medicine in Baltimore which is trialing a deep brain stimulator implant for Alzheimer’s patients was a little skeptical of the other team’s claims.

“The brain has a lot of redundancy, it can function pretty well if loses one or two parts. But memory involves circuits diffusely dispersed throughout the brain so it’s hard to envision.” However, he added that it was more likely to be successful in helping victims of stroke or localized brain injury as indeed its makers are aiming to do.

The UK’s Alzheimer’s Society is cautiously optimistic.

“Finding ways to combat symptoms caused by changes in the brain is an ongoing battle for researchers. An implant like this one is an interesting avenue to explore,” said Doug Brown, director of research and development.

Hampson says the team’s breakthrough is “like the difference between a cane, to help you walk, and a prosthetic limb — it’s two different approaches.”

It will still take time for many people to accept their findings and their claims, he says, but they don’t expect to have a shortage of volunteers stepping forward to try their implant — the project is partly funded by the U.S. military which is looking for help with battlefield injuries.

There are U.S. soldiers coming back from operations with brain trauma and a neurologist at DARPA (the Defense Advanced Research Projects Agency) is asking “what can you do for my boys?” Hampson says.

“That’s what it’s all about.”

http://www.cnn.com/2013/05/07/tech/brain-memory-implants-humans/index.html?iref=allsearch

Bionic superhumans on the horizon

1-bionic-hand-story-top

Around 220,000 people worldwide already walk around with cochlear implants — devices worn around the ear that turn sound waves into electrical impulses shunted directly into the auditory nerve.

Tens of thousands of people have been implanted with deep brain stimulators, devices that send an electrode tunneling several inches in the brain. Deep brain stimulators are used to control Parkinson’s disease, though lately they’ve also been tested — with encouraging results — in use against severe depression and obsessive compulsive disorder.

The most obvious bionics are those that replace limbs. Olympian “Blade Runner” Oscar Pistorius, now awaiting trial for the alleged murder of his girlfriend, made a splash with his Cheetah carbon fiber prostheses. Yet those are a relatively simple technology — a curved piece of slightly springy, super-strong material. In the digital age, we’re seeing more sophisticated limbs.

Consider the thought-controlled bionic leg that Zac Vawter used to climb all 103 floors of Chicago’s Willis Tower. Or the nerve-controlled bionic hand that Iraq war veteran Glen Lehman had attached after the loss of his original hand.

Or the even more sophisticated i-limb Ultra, an artificial hand with five independently articulating artificial fingers. Those limbs don’t just react mechanically to pressure. They actually respond to the thoughts and intentions of their owners, flexing, extending, gripping, and releasing on mental command.

The age when prostheses were largely inert pieces of wood, metal, and plastic is passing. Advances in microprocessors, in techniques to interface digital technology with the human nervous system, and in battery technology to allow prostheses to pack more power with less weight are turning replacement limbs into active parts of the human body.

In some cases, they’re not even part of the body at all. Consider the case of Cathy Hutchinson. In 1997, Cathy had a stroke, leaving her without control of her arms. Hutchinson volunteered for an experimental procedure that could one day help millions of people with partial or complete paralysis. She let researchers implant a small device in the part of her brain responsible for motor control. With that device, she is able to control an external robotic arm by thinking about it.

That, in turn, brings up an interesting question: If the arm isn’t physically attached to her body, how far away could she be and still control it? The answer is at least thousands of miles. In animal studies, scientists have shown that a monkey with a brain implant can control a robot arm 7,000 miles away. The monkey’s mental signals were sent over the internet, from Duke University in North Carolina, to the robot arm in Japan. In this day and age, distance is almost irrelevant.

The 7,000-mile-away prosthetic arm makes an important point: These new prostheses aren’t just going to restore missing human abilities. They’re going to enhance our abilities, giving us powers we never had before, and augmenting other capabilities we have. While the current generation of prostheses is still primitive, we can already see this taking shape when a monkey moves a robotic arm on the other side of the planet just by thinking about it.

Other research is pointing to enhancements to memory and decision making.

The hippocampus is a small, seahorse-shaped part of the brain that’s essential in forming new memories. If it’s damaged — by an injury to the head, for example — people start having difficulty forming new long-term memories. In the most extreme cases, this can lead to the complete inability to form new long-term memories, as in the film Memento. Working to find a way to repair this sort of brain damage, researchers in 2011 created a “hippocampus chip” that can replace damaged brain tissue. When they implanted it in rats with a damaged hippocampus, they found that not only could their chip repair damaged memory — it could improve the rats’ ability to learn new things.

Nor is memory the end of it. Another study, in 2012, demonstrated that we can boost intelligence — at least one sort — in monkeys. Scientists at Wake Forest University implanted specialized brain chips in a set of monkeys and trained those monkeys to perform a picture-matching game. When the implant was activated, it raised their scores by an average of 10 points on a 100-point scale. The implant makes monkeys smarter.

Both of those technologies for boosting memory and intelligence are in very early stages, in small animal studies only, and years (or possibly decades) away from wide use in humans. Still, they make us wonder — what happens when it’s possible to improve on the human body and mind?

The debate has started already, of course. Oscar Pistorius had to fight hard for inclusion in the Olympics. Many objected that his carbon fiber prostheses gave him a competitive advantage. He was able — with the help of doctors and biomedical engineers — to make a compelling case that his Cheetah blades didn’t give him any advantage on the field. But how long will that be true? How long until we have prostheses (not to mention drugs and genetic therapies) that make athletes better in their sports?

But the issue is much, much wider than professional sports. We may care passionately about the integrity of the Olympics or professional cycling or so on, but they only directly affect a very small number of us. In other areas of life — in the workforce in particular — enhancement technology might affect all of us.

When it’s possible to make humans smarter, sharper, and faster, how will that affect us? Will the effect be mostly positive, boosting our productivity and the rate of human innovation? Or will it be just another pressure to compete at work? Who will be able to afford these technologies? Will anyone be able to have their body, and more importantly, their brain upgraded? Or will only the rich have access to these enhancements?

We have a little while to consider these questions, but we ought to start. The technology will sneak its way into our lives, starting with people with disabilities, the injured, and the ill. It’ll improve their lives in ways that are unquestionably good. And then, one day, we’ll wake up and realize that we’re doing more than restoring lost function. We’re enhancing it.

Superhuman technology is on the horizon. Time to start thinking about what that means for us.

http://www.cnn.com/2013/04/24/opinion/bionic-superhumans-ramez-naam/index.html?iid=article_sidebar