Head injuries can make children loners

New research has found that a child’s relationships may be a hidden casualty long after a head injury.

Neuroscientists at Brigham Young University studied a group of children three years after each had suffered a traumatic brain injury – most commonly from car accidents. The researchers found that lingering injury in a specific region of the brain predicted the health of the children’s social lives.

“The thing that’s hardest about brain injury is that someone can have significant difficulties but they still look okay,” said Shawn Gale, a neuropsychologist at BYU. “But they have a harder time remembering things and focusing on things as well and that affects the way they interact with other people. Since they look fine, people don’t cut them as much slack as they ought to.”

Gale and Ph.D. student Ashley Levan authored a study to be published April 10 by the Journal of Head Trauma Rehabilitation, the leading publication in the field of rehabilitation. The study compared the children’s social lives and thinking skills with the thickness of the brain’s outer layer in the frontal lobe. The brain measurements came from MRI scans and the social information was gathered from parents on a variety of dimensions, such as their children’s participation in groups, number of friends and amount of time spent with friends.

A second finding from the new study suggests one potential way to help. The BYU scholars found that physical injury and social withdrawal are connected through something called “cognitive proficiency.” Cognitive proficiency is the combination of short-term memory and the brain’s processing speed.

“In social interactions we need to process the content of what a person is saying in addition to simultaneously processing nonverbal cues,” Levan said. “We then have to hold that information in our working memory to be able to respond appropriately. If you disrupt working memory or processing speed it can result in difficulty with social interactions.”

Separate studies on children with ADHD, which also affects the frontal lobes, show that therapy can improve working memory. Gale would like to explore in future research with BYU’s MRI facility if improvements in working memory could “treat” the social difficulties brought on by head injuries.

“This is a preliminary study but we want to go into more of the details about why working memory and processing speed are associated with social functioning and how specific brain structures might be related to improve outcome,” Gale said.

Kids’ earliest memories might be earlier than they think

The very earliest childhood memories might begin even earlier than anyone realized – including the rememberer, his or her parents and memory researchers.

Four- to 13-year-olds in upstate New York and Newfoundland, Canada, probed their memories when researchers asked: “You know, some kids can remember things that happened to them when they were very little. What is the first thing you can remember? How old were you at that time?” The researchers then returned a year or two later to ask again about earliest memories – and at what age the children were when the events occurred.

“The age estimates of earliest childhood memories are not as accurate as what has been generally assumed,” report Qi Wang of Cornell University and Carole Peterson of Memorial University of Newfoundland in the March 2014 online issue of Developmental Psychology. “Using children’s own age estimates as the reference, we found that memory dating shifted to later ages as time elapsed.”

Childhood amnesia refers to our inability to remember events from our first years of life. Until now, cognitive psychologists estimated the so-called childhood amnesia offset at 3.5 years – the average age of our very earliest memory, the authors noted in their report, “Your Earliest Memory May Be Earlier Than You Think: Prospective Studies of Children’s Dating of Earliest Childhood Memories.”

But the children who originally answered, for example, “I think I was 3 years old when my dog fell through the ice,” postdated that same earliest memory by as much as nine months when asked – in follow-up interviews a year or two years later – to recall again. In other words, as time went by, children thought the same memory event occurred at an older age than they had thought previously. And that finding prompts Wang and Peterson to question the 3.5-year offset for childhood amnesia.

“This can happen to adults’ earliest childhood memories, too,” says Wang, professor of human development and director of the Social Cognition Development Laboratory in Cornell’s College of Human Ecology. “We all remember some events from our childhood. When we try to reconstruct the time of these events, we may postdate them to be more recent than they actually were, as if we are looking at the events through a telescope. Although none of us can recall events on the day of our birth – childhood amnesia may end somewhat earlier than the generally accepted 3.5 years.”

Parents might help because they have more clues (e.g., where they lived, what their children looked like at the time of events) to put their children’s experiences along a timeline. When asked, for example, “How old was Evan when Poochie fell through the ice?” they erred less than Evan had. Still, they are not free from errors in their time estimates.

The only way to settle that, Wang and Peterson mused, would be to look for documented evidence – a parent’s diary, for instance, or a newspaper account of Poochie’s memorable rescue.

Brain activity drives dynamic changes in neural fiber insulation

The brain is a wonderfully flexible and adaptive learning tool. For decades, researchers have known that this flexibility, called plasticity, comes from selective strengthening of well-used synapses — the connections between nerve cells.

Now, researchers at the Stanford University School of Medicine have demonstrated that brain plasticity also comes from another mechanism: activity-dependent changes in the cells that insulate neural fibers and make them more efficient. These cells form a specialized type of insulation called myelin.

“Myelin plasticity is a fascinating concept that may help to explain how the brain adapts in response to experience or training,” said Michelle Monje, MD, PhD, assistant professor of neurology and neurological sciences.

The researchers’ findings are described in a paper published online April 10 in Science Express.

“The findings illustrate a form of neural plasticity based in myelin, and future work on the molecular mechanisms responsible may ultimately shed light on a broad range of neurological and psychiatric diseases,” said Monje, senior author of the paper. The lead authors of the study are Stanford postdoctoral scholar Erin Gibson, PhD, and graduate student David Purger.

Sending neural impulses quickly down a long nerve fiber requires insulation with myelin, which is formed by a cell called an oligodendrocyte that wraps itself around a neuron. Even small changes in the structure of this insulating sheath, such as changes in its thickness, can dramatically affect the speed of neural-impulse conduction. Demyelinating disorders, such as multiple sclerosis, attack these cells and degrade nerve transmission, especially over long distances.

Myelin-insulated nerve fibers make up the “white matter” of the brain, the vast tracts that connect one information-processing area of the brain to another. “If you think of the brain’s infrastructure as a city, the white matter is like the roads, highways and freeways that connect one place to another,” Monje said.

In the study, Monje and her colleagues showed that nerve activity prompts oligodendrocyte precursor cell proliferation and differentiation into myelin-forming oligodendrocytes. Neuronal activity also causes an increase in the thickness of the myelin sheaths within the active neural circuit, making signal transmission along the neural fiber more efficient. It’s much like a system for improving traffic flow along roadways that are heavily used, Monje said. And as with a transportation system, improving the routes that are most productive makes the whole system more efficient.

In recent years, researchers have seen clues that nerve cell activity could promote the growth of myelin insulation. There have been studies that showed a correlation between experience and myelin dynamics, and studies of isolated cells in a dish suggesting a relationship between neuronal activity and myelination. But there has been no way to show that neuronal activity directly causes myelin changes in an intact brain. “You can’t really implant an electrode in the brain to answer this question because the resulting injury changes the behavior of the cells,” Monje said.

The solution was a relatively new and radical technique called optogenetics. Scientists insert genes for a light-sensitive ion channel into a specific group of neurons. Those neurons can be made to fire when exposed to particular wavelengths of light. In the study, Monje and her colleagues used mice with light-sensitive ion channels in an area of their brains that controls movement. The scientists could then turn on and off certain movement behaviors in the mice by turning on and off the light. Because the light diffuses from a source placed at the surface of the brain down to the neurons being studied, there was no need to insert a probe directly next to the neurons, which would have created an injury.

By directly stimulating the neurons with light, the researchers were able to show it was the activation of the neurons that prompted the myelin-forming cells to respond.

Further research could reveal exactly how activity promotes oligodendrocyte-precursor-cell proliferation and maturation, as well as dynamic changes in myelin. Such a molecular understanding could help researchers develop therapeutic strategies that promote myelin repair in diseases in which myelin is degraded, such as multiple sclerosis, the leukodystrophies and spinal cord injury.

“Conversely, when growth of these cells is dysregulated, how does that contribute to disease?” Monje said. One particular area of interest for her is a childhood brain cancer called diffuse intrinsic pontine glioma. The cancer, which usually strikes children between 5 and 9 years old and is inevitably fatal, occurs when the brain myelination that normally takes place as kids become more physically coordinated goes awry, and the brain cells grow out of control.

Researchers search for earliest roots of psychiatric disorders

Newborns whose mothers were exposed during pregnancy to any one of a variety of environmental stressors — such as trauma, illness, and alcohol or drug abuse — become susceptible to various psychiatric disorders that frequently arise later in life. However, it has been unclear how these stressors affect the cells of the developing brain prenatally and give rise to conditions such as schizophrenia, post-traumatic stress disorder, and some forms of autism and bipolar disorders. 

Now, Yale University researchers have identified a single molecular mechanism in the developing brain that sheds light on how cells may go awry when exposed to a variety of different environmental insults. The findings, to be published in the May 7 issue of the journal Neuron, suggest that different types of stressors prenatally activate a single molecular trigger in brain cells that may make exposed individuals susceptible to late-onset neuropsychiatric disorders.

The researchers found that mouse embryos exposed to alcohol, methyl-mercury, or maternal seizures all activate in the developing brain cells a single gene — HSF1 or heat shock factor — which protects and enables some of the brain cells to survive prenatal insult. Mice lacking the HSF1 gene showed structural brain abnormalities and were prone to seizures after birth, even after exposure to very low levels of the toxins.

In addition, researchers created stem cells — which are capable of becoming many different tissue types, including neurons — from biopsies of individuals diagnosed with schizophrenia. Genes from these “schizophrenic” stem cells responded more dramatically when exposed to environmental insults than stem cells obtained from non-schizophrenic individuals. The findings provide support to the thesis that stress induces vulnerable cells to malfunction.

“It appears that different types of environmental stressors can trigger the same condition if they occur at the same period of prenatal development,” said Yale’s Pasko Rakic, senior author of the study. “Conversely, the same environmental stressor may cause different pathologies, if it occurs at different times during pregnancy.”

Since HSF1 activation can potentially serve as a permanent marker of the stressed/damaged cell, it opens the possibility of identifying these cells in adults in order to explore the pathogenesis of postnatal disorders and how to protect vulnerable cells.

(Image caption: Olfactory sensory neurons (green and magenta) located in the olfactory epithelium. Credit: Image courtesy of Limei Ma, Ph.D., Stowers Institute for Medical Research)

Finding the target: how timing is critical in establishing an olfactory wiring map

The human nose expresses nearly 400 odorant receptors, which allow us to distinguish a large number of scents. In mice the number of odor receptors is closer to 1000. Each olfactory neuron displays only a single type of receptor and all neurons with the same receptors are connected to the same spot, a glomerulus, in the brain. This convergence, or wiring pattern, is often described as an olfactory map. The map is important because it serves as a code book for odorants that allows the brain to distinguish between food odors and the scent of a predator, among others.

Unlike photoreceptors in the retina or hair cells in the inner ear, which cannot be replaced once damaged, olfactory neurons have the unique capacity to regenerate throughout the life. More remarkably, the regenerated neurons must dispatch their axons on a path through the nasal epithelium to the brain through a distance a thousand times the length of the cell, where they make the proper connections. If regenerating neurons are mis-wired to different glomeruli, odor perception would be altered.

In the April 11, 2014 issue of Science, Associate Investigator C. Ron Yu, Ph.D. and colleagues at the Stowers Institute of Medical Research identify a developmental window during which olfactory neurons of newborn mice can form a proper wiring map. They show that if incorrect neuronal connections are maintained after this period, renewing cells will also be mis-wired.

Their results also hint at how the olfactory neurons connect to their targets. Although scientists can induce stem cells to become neurons, they know little about how to precisely steer them to make the proper connections. This work suggests additional targeting skills that stem cell-generated neurons need to acquire to repair the brain or spinal cord.

Previously, researchers thought that since olfactory neurons exhibited lifelong regeneration, they likewise retained the ability to re-establish correct connections. “We show that this is not the case,” says Yu. In the report, his team uses a number of transgenic mouse lines to demonstrate that the first week after birth is a critical window of time during which incorrect projections can be restored to normal. “If mis-targeting does not get corrected within this period, cells still regenerate but many get locked onto the wrong tracks.” Yu adds.

Neuronal wiring has intrigued Yu since he was a post-doc in the lab of Richard Axel, M.D., at Columbia University. Back then Yu created a genetically engineered mouse in which he could temporarily muffle the firing of olfactory neurons. He found that inactivating neurons caused them to connect to the wrong glomeruli. After joining the Stowers Institute in 2005, Yu began to wonder whether an incorrectly wired olfactory map could be restored in mice.

In this new work, Yu’s team, led by first author Limei Ma, Ph.D., reports that if the silenced sensory neurons are reactivated within a week of a mouse’s birth, erroneous olfactory neuron connections are restored. Beyond that critical period, however, neurons appeared to lose the capacity to make the right connections and in fact maintained connections to the wrong glomeruli.

“After the first week, we believe that newly generated neurons follow pre-existing tracks to their target,” says Ma, Senior Research Specialist in the Yu lab. A key finding in the report supports this idea. The team provoked a temporary identity crisis in olfactory neurons by broadly mis-expressing an odorant receptor called M71 in cells where it would not normally be displayed. Surprisingly, only the neurons that normally express the M71 receptor targeted the “wrong” glomeruli, not the neurons that express different odorant receptors. 

An interpretation of this experiment is that late-born olfactory neurons expressing a particular receptor recognize and follow a track laid down earlier by neurons expressing the very same receptor—even if the latter expressed that receptor due to experimental manipulation. “These olfactory neurons have identity tags,” says Ma, referring to the receptors. “And they like to follow others displaying the same tag.”

As yet, investigators have not identified the molecular basis for the targeting switch occurring at the end of one-week period. “We don’t know what keeps these late stage cells from re-establishing the right connections,” explains Ma. “Either the cues that guide them disappear or their axons encounter a physical barrier to the target.”

Yu envisions the studies in the olfactory system will provide clues on how a regenerated neuron, either through a natural process in the case of the olfactory neuron, or by stem technology, find their target and make the right connection. “To repair a damaged spinal cord, you will need to ensure that newly generated motor neurons target the right muscle,” says Yu. “The next goal is to identify the molecular cues that enable correct projections to be established.”

(Image caption: A window of plasticity. Native neurons (green) that express the odorant receptor MOR28 attach to known glomeruli (above). Neurons expressing engineered MOR28 (red) may attach to other glomeruli. Growing side-by-side, the red neurons could redirect some of the green, but only in the perinatal period. Neuron wiring established early remained stable in adults. Credit: Barnea lab/Brown University)

Early neural wiring for smell persists

A new study in Science reveals that the fundamental wiring of the olfactory system in mice sets up shortly after birth and then remains stable but adaptable. The research highlights how important early development can be throughout life and provides insights that may be important in devising regenerative medical therapies in the nervous system.

To accommodate a lifetime of scents and aromas, mammals have hundreds of genes that each produce a different odorant receptor. The complex and diverse olfactory system they build remains adaptable, but a new study in the journal Science shows that the system’s flexibility, or plasticity, has its limits. Working in mice, Brown University scientists found that the fundamental neural wiring map between the nose and the brain becomes established in a critical period of early development and then regenerates the same map thereafter.

The findings not only reveal a key moment with lifelong consequences in the development of a vital sensory system, but also may provide a “heads up” for bioengineers and doctors looking to develop regenerative therapies for the central nervous system. As flexible as the brain is, it also has mechanisms — at least in the olfactory system — to ensure that the connections established early will be maintained for life.

“Our experiments enabled us to reveal that the system has some ‘memory’,” said Gilad Barnea, the Robert and Nancy Carney Assistant Professor of Neuroscience and corresponding author of the study.

Tracking connections

Lead author Lulu Tsai, now a postdoctoral fellow at Drexel University, conducted the experiments under Barnea’s supervision while she was a graduate student at Brown. Tsai and Barnea are the paper’s only authors.

“Lulu really sweated for this,” Barnea said. “These experiments were very complicated.”

Tsai and Barnea sought to track the development of sensory neurons that express an odorant receptor, MOR28, through space and time in the mouse olfactory system. They did so by engineering a version of the receptor that could be expressed or suppressed at key developmental times. Neurons that express the engineered version of MOR28 would glow red under the microscope. In addition, the researchers tweaked the native version of the receptor gene such that neurons that express it would glow green.

In a typical mammalian olfactory system, neurons expressing a receptor gene like MOR28 will be found randomly sprinkled around the lining of the nose, but their long, wiry axons will all connect to just two symmetrical pairs of structures called glomeruli within the brain’s olfactory bulb. The glomeruli relay odor signals to the rest of the brain.

Barnea and Tsai’s mice developed similarly, with most native MOR28-expressing neurons connecting their axons into the typical glomeruli during early development. But when the researchers let the engineered MOR28 become expressed, those connected into other nearby glomeruli. Significantly, native MOR28 axons sometimes ended up becoming rerouted to these alternate glomeruli with their engineered brethren. Under the microscope, green mixed with red.

It’s a novel finding that some engineered MOR28-expressing neurons could reroute native MOR28-expressing neurons to join them outside the standard four MOR28 glomeruli. It suggests that olfactory neurons influence each other during early development as they find their way to glomeruli and don’t, as current neurodevelopmental models suggest, do so autonomously.

Timing is everything

But the main finding of a critical period where wiring becomes locked in came about as Tsai controlled the timing of engineered MOR28 receptor expression. She induced that on the day some mice were born, a week later in other mice, and two weeks later in still others. In mice where engineered MOR28 expression was allowed at birth, one in nine mice showed rerouting of native MOR28 axons to glomeruli with engineered MOR28. A week out only one in 17 mice showed any rerouting. After two weeks it never happened.

“We conclude that there is a critical period for the formation of rerouted-MOR28 glomeruli that ends at birth or shortly thereafter,” Tsai and Barnea wrote in Science.

The researchers also looked at this in other ways. In one experiment, they found that they didn’t need to maintain expression of the engineered MOR28 for the rerouted connections to persist into adulthood. Once established, they remained.

They also tested whether the rerouting seen in developing mice could occur in adults. They let native MOR28-expressing axons grow alone, and then wiped them out. Then they let native and engineered MOR28-expressing neurons regrow fresh connections to the olfactory bulb together when the mice were adults. They never saw rerouting in the adult mice as connections regrew, suggesting that the ability to reroute is lost in adulthood.

In yet another experiment, they found that if they let rerouted glomeruli become established and then wiped out olfactory neurons, the regrowing connections would return to the rerouted glomeruli even when the engineered receptor was no longer expressed. So although adults can’t create new rerouted glomeruli, they will restore existing ones.

All of the experiments together showed that the fundamental wiring diagram of the olfactory system is laid out and implemented early in life. Whatever pattern is established then stays there for life.

These observations suggest that the course of early development has lifelong consequences, Barnea said, providing insight into understanding of neurodevelopmental and psychiatric disorders.

These observations may also have implications for regenerative medicine, Barnea said. Once neural circuits are established, it may be difficult to induce subsequent fundamental alterations to them. On the other hand, learning more about the differences between early development and the adult system may help to devise better regenerative strategies.

“It is clear that there is much more for us to learn about the development of neural circuits,” he said.

How the brain pays attention

Neuroscientists identify a brain circuit that’s key to shifting our focus from one object to another.

Picking out a face in the crowd is a complicated task: Your brain has to retrieve the memory of the face you’re seeking, then hold it in place while scanning the crowd, paying special attention to finding a match.

A new study by MIT neuroscientists reveals how the brain achieves this type of focused attention on faces or other objects: A part of the prefrontal cortex known as the inferior frontal junction (IFJ) controls visual processing areas that are tuned to recognize a specific category of objects, the researchers report in the April 10 online edition of Science.

Scientists know much less about this type of attention, known as object-based attention, than spatial attention, which involves focusing on what’s happening in a particular location. However, the new findings suggest that these two types of attention have similar mechanisms involving related brain regions, says Robert Desimone, the Doris and Don Berkey Professor of Neuroscience, director of MIT’s McGovern Institute for Brain Research, and senior author of the paper.

“The interactions are surprisingly similar to those seen in spatial attention,” Desimone says. “It seems like it’s a parallel process involving different areas.”

In both cases, the prefrontal cortex — the control center for most cognitive functions — appears to take charge of the brain’s attention and control relevant parts of the visual cortex, which receives sensory input. For spatial attention, that involves regions of the visual cortex that map to a particular area within the visual field.

In the new study, the researchers found that IFJ coordinates with a brain region that processes faces, known as the fusiform face area (FFA), and a region that interprets information about places, known as the parahippocampal place area (PPA). The FFA and PPA were first identified in the human cortex by Nancy Kanwisher, the Walter A. Rosenblith Professor of Cognitive Neuroscience at MIT.  

The IFJ has previously been implicated in a cognitive ability known as working memory, which is what allows us to gather and coordinate information while performing a task — such as remembering and dialing a phone number, or doing a math problem.

For this study, the researchers used magnetoencephalography (MEG) to scan human subjects as they viewed a series of overlapping images of faces and houses. Unlike functional magnetic resonance imaging (fMRI), which is commonly used to measure brain activity, MEG can reveal the precise timing of neural activity, down to the millisecond. The researchers presented the overlapping streams at two different rhythms — two images per second and 1.5 images per second — allowing them to identify brain regions responding to those stimuli.

“We wanted to frequency-tag each stimulus with different rhythms. When you look at all of the brain activity, you can tell apart signals that are engaged in processing each stimulus,” says Daniel Baldauf, a postdoc at the McGovern Institute and the lead author of the paper.

Each subject was told to pay attention to either faces or houses; because the houses and faces were in the same spot, the brain could not use spatial information to distinguish them. When the subjects were told to look for faces, activity in the FFA and the IFJ became synchronized, suggesting that they were communicating with each other. When the subjects paid attention to houses, the IFJ synchronized instead with the PPA.

The researchers also found that the communication was initiated by the IFJ and the activity was staggered by 20 milliseconds — about the amount of time it would take for neurons to electrically convey information from the IFJ to either the FFA or PPA. The researchers believe that the IFJ holds onto the idea of the object that the brain is looking for and directs the correct part of the brain to look for it.

The MEG scanner, as well as the study’s “elegant design,” were critical to discovering this relationship, says Robert Knight, a professor of psychology and neuroscience at the University of California at Berkeley who was not part of the research team.

“Functional MRI gives hints of connectivity,” Knight says, “but the time course is way too slow to show these millisecond-scale frequencies and to establish what they show, which is that the inferior frontal lobe is the prime driver.”

Further bolstering this idea, the researchers used an MRI-based method to measure the white matter that connects different brain regions and found that the IFJ is highly connected with both the FFA and PPA.

Members of Desimone’s lab are now studying how the brain shifts its focus between different types of sensory input, such as vision and hearing. They are also investigating whether it might be possible to train people to better focus their attention by controlling the brain interactions  involved in this process.

“You have to identify the basic neural mechanisms and do basic research studies, which sometimes generate ideas for things that could be of practical benefit,” Desimone says. “It’s too early to say whether this training is even going to work at all, but it’s something that we’re actively pursuing.”

The effects of working memory training on functional brain network efficiency

The human brain is a highly interconnected network. Recent studies have shown that the functional and anatomical features of this network are organized in an efficient small-world manner that confers high efficiency of information processing at relatively low connection cost. However, it has been unclear how the architecture of functional brain networks is related to performance in working memory (WM) tasks and if these networks can be modified by WM training. Therefore, we conducted a double-blind training study enrolling 66 young adults. Half of the subjects practiced three WM tasks and were compared to an active control group practicing three tasks with low WM demand. High-density resting-state electroencephalography (EEG) was recorded before and after training to analyze graph-theoretical functional network characteristics at an intracortical level. WM performance was uniquely correlated with power in the theta frequency, and theta power
was increased by WM training. Moreover, the better a person’s WM performance, the more their network exhibited small-world topology. WM training shifted network characteristics in the direction of high performers, showing increased small-worldness within a distributed fronto-parietal network. Taken together, this is the first longitudinal study that provides evidence for the plasticity of the functional brain network underlying WM.

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New Studies Show Promise for Brain Training in Improving Fluid Intelligence

Whether computerized games designed by psychologists and neuroscientists can literally make people smarter has been hotly debated by scientists, with a small but outspoken cadre of skeptics demanding stronger proof. Now two new studies have found the kind of real-world benefits from the brain-training games that skeptics have been calling for.

The first, published today in the Proceedings of the National Academy of Sciences, found that less than six hours of brain games played over the course of 10 weeks enabled poor first-graders who attend school irregularly due to family problems to catch up with their regularly-attending peers in math and language grades.

The second, presented over the weekend at the Cognitive Neuroscience Society meeting in Boston, combined the results of 13 previous studies of computerized brain-training in young adults to conclude that training significantly enhances fluid intelligence—the fundamental human ability to detect patterns, reason, and learn.  That is, practicing the games literally makes people smarter.  

Together with other recent studies demonstrating real-world benefits of brain training in healthy older adults, preschoolers, and school children with ADHD, the new papers appear to provide fresh ammunition to psychologists and neuroscientists whose research has been under attack by a handful of skeptics who insist that the training is a waste of time.

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Regular aerobic exercise boosts memory area of brain in older women

Regular aerobic exercise seems to boost the size of the area of the brain (hippocampus) involved in verbal memory and learning among women whose intellectual capacity has been affected by age, indicates a small study published online in the British Journal of Sports Medicine.

The hippocampus has become a focus of interest in dementia research because it is the area of the brain involved in verbal memory and learning, but it is very sensitive to the effects of ageing and neurological damage.

The researchers tested the impact of different types of exercise on the hippocampal volume of 86 women who said they had mild memory problems, known as mild cognitive impairment - and a common risk factor for dementia.

All the women were aged between 70 and 80 years old and were living independently at home.

Roughly equal numbers of them were assigned to either twice weekly hour long sessions of aerobic training (brisk walking); or resistance training, such as lunges, squats, and weights; or balance and muscle toning exercises, for a period of six months.

The size of their hippocampus was assessed at the start and the end of the six month period by means of an MRI scan, and their verbal memory and learning capacity was assessed before and afterward using a validated test (RAVLT).

Only 29 of the women had before and after MRI scans, but the results showed that the total volume of the hippocampus in the group who had completed the full six months of aerobic training was significantly larger than that of those who had lasted the course doing balance and muscle toning exercises.

No such difference in hippocampal volume was seen in those doing resistance training compared with the balance and muscle toning group.

However, despite an earlier finding in the same sample of women that aerobic exercise improved verbal memory, there was some evidence to suggest that an increase in hippocampal volume was associated with poorer verbal memory.

This suggests that the relationship between brain volume and cognitive performance is complex, and requires further research, say the authors.

But at the very least, aerobic exercise seems to be able to slow the shrinkage of the hippocampus and maintain the volume in a group of women who are at risk of developing dementia, they say.

And they recommend regular aerobic exercise to stave off mild cognitive decline, which is especially important, given the mounting evidence showing that regular exercise is good for cognitive function and overall brain health, and the rising toll of dementia.

Worldwide, one new case of dementia is diagnosed every four seconds, with the number of those afflicted set to rise to more than 115 million by 2050, they point out.