Posts tagged learning
Articles and news from the latest research reports.
During pregnancy, the bone hormone osteocalcin is produced by the mother; it crosses the placenta, to reach the fetus, where it promotes the formation of the hippocampus and the development of spatial learning and memory. Postnatally, osteocalcin crosses the blood-brain barrier (BBB), to act in various regions of the brain, including the hippocampus, where it causes changes in brain chemistry that help prevent anxiety and depression and improve spatial learning and memory.
Image credit: Gerard Karsenty, MD, PhD and Franck Oury, PhD/Columbia University Medical Center
Bone Hormone Influences Brain Development and Cognition
Findings could lead to new treatments for memory loss, anxiety, and depression
Researchers from Columbia University Medical Center (CUMC) have found that the skeleton, acting through the bone-derived hormone osteocalcin, exerts a powerful influence on prenatal brain development and cognitive functions such as learning, memory, anxiety, and depression in adult mice. Findings from the mouse study could lead to new approaches to the prevention and treatment of neurologic disorders. The study was published today in the online edition of Cell.
“The brain is commonly viewed as an organ that influences other organs and parts of the body, but less often as the recipient of signals coming from elsewhere, least of all, the bones,” said study leader Gerard Karsenty, MD, PhD, Paul A. Marks Professor of Genetics and Development, professor of medicine, and chair of the Department of Genetics and Development.
“In an earlier study, we showed that the brain is a powerful inhibitor of bone mass accrual,” he said. “This effect was so powerful that it immediately raised the question, ‘Does the bone signal back to the brain to limit this negative influence?’ ‘If so, what signals does it use and how do they work?’”
Dr. Karsenty suspected that osteocalcin, a hormone recently identified by his lab and secreted by osteoblasts, might be involved in such bone-to-brain signaling. Earlier studies had shown that osteocalcin affects a variety of processes, such as energy expenditure, glucose balance, and male fertility. “Since most hormones influence a range of physiological processes, it was reasonable to assume that the endocrine functions of osteocalcin were even broader than what was already known,” he said.
To determine whether osteocalcin did indeed play a role in the brain, Dr. Karsenty and his team studied “osteocalcin-null” mice (mice that have been genetically engineered to not produce any osteocalcin). Using these mice, they were able to show unambiguously that osteocalcin can cross the blood-brain barrier; binds to neurons in the brainstem, midbrain, and hippocampus (which is responsible for learning and memory); promotes the birth of neurons; and increases the synthesis of several neurotransmitters, including serotonin, dopamine, and catecholamine. They also found that osteocalcin-null mice had abnormally small hippocampi, a part of the brain involved in memory.
The researchers then hypothesized that the changes in neurotransmitter synthesis should alter the animals’ behavior. In a series of behavioral tests, they confirmed that osteocalcin-null mice exhibit increased anxiety and depression-like behaviors, as well as impaired learning and memory, compared with normal mice.
These changes are similar to those seen in the aging population. “As we age, bone mass decreases, and the production of osteocalcin probably does, too,” said Dr. Karsenty. “We’re currently looking into this. It is not inconceivable that treatments that boost osteocalcin levels or stimulate osteocalcin receptors could help counter the cognitive effects of aging and aging-related diseases such as Alzheimer’s.”
When adult osteocalcin-null mice were infused with osteocalcin, their anxiety and depression did decrease, “but the infusions didn’t affect learning and memory or the size of the hippocampus,” said Dr. Karsenty. “This was perplexing, so we did another experiment—a postnatal knockout of osteocalcin (a genetically engineered model in which the synthesis of osteocalcin is blocked after birth). These mice were anxious and depressed but had normal memory and hippocampus structure. The unavoidable conclusion of the two experiments was that osteocalcin must act during development.” This led to the second part of their study.
In subsequent experiments, the researchers showed that osteocalcin crosses the placenta from mother to fetus and that this maternal pool of osteocalcin is necessary for formation of the hippocampus and the establishment of memory. Lastly, they showed that once-a-day injections of osteocalcin in osteocalcin-null mothers during pregnancy could prevent the development of behavioral abnormalities in their offspring.
“This finding could explain some of the effects observed in children born from undernourished mothers who develop, with an unusually high frequency, metabolic and psychiatric disorders just as osteocalcin-null mice do,” said Dr. Karsenty. “Malnutrition decreases the activity of bone cells; as a result, undernourished mothers have low bone mass, which affects osteocalcin production. This has clinical relevance even today, in developing countries, where maternal malnutrition is still common.”
Any therapies related to osteocalcin are still years away, however, he added.
Getting an expected award music to the brain’s ears
Several studies have shown that expecting a reward or punishment can affect brain activity in areas responsible for processing different senses, including sight or touch. For example, research shows that these brain regions light up on brain scans when humans are expecting a treat. However, researchers know less about what happens when the reward is actually received—or an expected reward is denied. Insight on these scenarios can help researchers better understand how we learn in general.
To get a better grasp on how the brain behaves when people who are expecting a reward actually receive it, or conversely, are denied it, Tina Weis of Carl-von-Ossietzky University and her colleagues monitored the auditory cortex—the part of the brain that processes and interprets sounds—while volunteers solved a task in which they had a chance of winning 50 Euro cents with each round, signaled by a specific sound. Their findings show that the auditory cortex activity picked up both when participants were expecting a reward and received it, as well as when their expectation of receiving no reward was correct.
The article is entitled “Feedback that Confirms Reward Expectation Triggers Auditory Cortex Activity.” It appears in the Articles in Press section of the Journal of Neurophysiology, published by the American Physiological Society.
Methodology
The researchers worked with 105 healthy adult volunteers with normal hearing. While each volunteer received a functional MRI (fMRI)—a brain scan that measures brain activity during tasks—the researchers had them solve a task with sounds where they had the chance of winning money at the end of each round. At the beginning of a round participants heard a sound and had to learn if this sound signified that they could win a 50 Euro cents reward or not. They then saw a number on a screen and had to press a button to indicate whether the number was greater or smaller than 5. If the sound before indicated that they could receive a reward and they solved the number task quickly and correctly, an image of a 50 Euro cents coin appeared on the screen. The researchers monitored brain activity in the subjects’ auditory cortex throughout the task, paying special attention to what happened when they received the reward, or not, at the end of the round.
Results
The study authors found that when the volunteers were expecting and finally received a reward, then their auditory cortex was activated. Similarly, there was an increase in brain activity in this area when the subjects weren’t expecting a reward and didn’t get one. There was no additional activity when they were expecting a reward and didn’t get one.
Importance of the Findings
These findings add to accumulating evidence that the auditory cortex performs a role beyond just processing sound. Rather, this area of the brain appears to be activated during other activities that require learning and thought, such as confirming expectations of receiving a reward.
"Our findings thus support the view of a highly cognitive role of the auditory cortex," the study authors say.
(Source: eurekalert.org)
Study finds link between commonly prescribed statin and memory impairment
New research that looked at whether two commonly prescribed statin medicines, used to lower low-density lipoprotein (LDL) or‘bad cholesterol’ levels in the blood, can adversely affect cognitive function has found that one of the drugs tested caused memory impairment in rats.
Between six and seven million people in the UK take statins daily and the findings follow anecdotal evidence of people reporting that they feel that their newly prescribed statin is affecting their memory. Last year, the US Food and Drug Administration (FDA) insisted that all manufacturers list in their side effects that statins might affect cognitive function.
The study, led by scientists at the University of Bristol and published in the journal PLOS ONE, tested pravastatin and atorvostatin (two commonly prescribed statins) in rat learning and memory models. The findings show that while no adverse cognitive effects were observed in rat performance for simple learning and memory tasks for atorvostatin, pravastatin impaired their performance.
Rats were treated daily with pravastatin (brand name - Pravachol) or atorvostatin (brand name - Lipitor) for 18 days. The rodents were tested in a simple learning task before, during and after treatment, where they had to learn where to find a food reward. On the last day of treatment and following one week withdrawal, the rats were also tested in a task which measures their ability to recognise a previously encountered object (recognition memory).
The study’s findings showed that pravastatin tended to impair learning over the last few days of treatment although this effect was fully reversed once treatment ceased. However, in the novel object discrimination task, pravastatin impaired object recognition memory. While no effects were observed for atorvostatin in either task.
The results suggest that chronic treatment with pravastatin impairs working and recognition memory in rodents. The reversibility of the effects on stopping treatment is similar to what has been observed in patients, but the lack of effect of atorvostatin suggests that some types of statin may be more likely to cause cognitive impairment than others.
Neil Marrion, Professor of Neuroscience at Bristol’s School of Physiology and Pharmacology in the Faculty of Medical and Veterinary Sciences and the study’s lead author, said: “This finding is novel and likely reflects both the anecdotal reports and FDA advice. What is most interesting is that it is not a feature of all statins. However, in order to better understand the relationship between statin treatment and cognitive function, further studies are needed.”
(Source: bris.ac.uk)
Scientists Pinpoint Proteins Vital to Long-Term Memory
Scientists from the Florida campus of The Scripps Research Institute (TSRI) have found a group of proteins essential to the formation of long-term memories.
The study, published online ahead of print on September 12, 2013 by the journal Cell Reports, focuses on a family of proteins called Wnts. These proteins send signals from the outside to the inside of a cell, inducing a cellular response crucial for many aspects of embryonic development, including stem cell differentiation, as well as for normal functioning of the adult brain.
“By removing the function of three proteins in the Wnt signaling pathway, we produced a deficit in long-term but not short-term memory,” said Ron Davis, chair of the TSRI Department of Neuroscience. “The pathway is clearly part of the conversion of short-term memory to the long-term stable form, which occurs through changes in gene expression.”
The findings stem from experiments probing the role of Wnt signaling components in olfactory memory formation in Drosophila, the common fruit fly—a widely used doppelgänger for human memory studies. In the new study, the scientists inactivated the expression of several Wnt signaling proteins in the mushroom bodies of adult flies—part of the fly brain that plays a role in learning and memory.
The resulting memory disruption, Davis said, suggests that Wnt signaling participates actively in the formation of long-term memory, rather than having some general, non-specific effect on behavior.
“What is interesting is that the molecular mechanisms of adult memory use the same processes that guide the early development of the organism, except that they are repurposed for memory formation,” he said. “One difference, however, is that during early development the signals are intrinsic, while in adults they require an outside stimulus to create a memory.”
(Source: scripps.edu)
Researchers discover how inhibitory neurons behave during critical periods of learning
We’ve all heard the saying “you can’t teach an old dog new tricks.” Now neuroscientists are beginning to explain the science behind the adage.
For years, neuroscientists have struggled to understand how the microcircuitry of the brain makes learning easier for the young, and more difficult for the old. New findings published in the journal Nature by Carnegie Mellon University, the University of California, Los Angeles and the University of California, Irvine show how one component of the brain’s circuitry — inhibitory neurons — behave during critical periods of learning.
The brain is made up of two types of cells — inhibitory and excitatory neurons. Networks of these two kinds of neurons are responsible for processing sensory information like images, sounds and smells, and for cognitive functioning. About 80 percent of neurons are excitatory. Traditional scientific tools only allowed scientists to study the excitatory neurons.
"We knew from previous studies that excitatory cells propagate information. We also knew that inhibitory neurons played a critical role in setting up heightened plasticity in the young, but ideas about what exactly those cells were doing were controversial. Since we couldn’t study the cells, we could only hypothesize how they were behaving during critical learning periods," said Sandra J. Kuhlman, assistant professor of biological sciences at Carnegie Mellon and member of the joint Carnegie Mellon/University of Pittsburgh Center for the Neural Basis of Cognition.
The prevailing theory on inhibitory neurons was that, as they mature, they reach an increased level of activity that fosters optimal periods of learning. But as the brain ages into adulthood and the inhibitory neurons continue to mature, they become even stronger to the point where they impede learning.
Newly developed genetic and imaging technologies are now allowing researchers to visualize inhibitory neurons in the brain and record their activity in response to a variety of stimuli. As a postdoctoral student at UCLA in the laboratory of Associate Professor of Neurobiology Joshua T. Trachtenberg, Kuhlman and her colleagues used these new techniques to record the activity of inhibitory neurons during critical learning periods. They found that, during heightened periods of learning, the inhibitory neurons didn’t fire more as had been expected. They fired much less frequently — up to half as often.
"When you’re young you haven’t experienced much, so your brain needs to be a sponge that soaks up all types of information. It seems that the brain turns off the inhibitory cells in order to allow this to happen," Kuhlman said. "As adults we’ve already learned a great number of things, so our brains don’t necessarily need to soak up every piece of information. This doesn’t mean that adults can’t learn, it just means when they learn, their neurons need to behave differently."
Study in mice links cocaine use to new brain structures
Mice given cocaine showed rapid growth in new brain structures associated with learning and memory, according to a research team from the Ernest Gallo Clinic and Research Center at UC San Francisco. The findings suggest a way in which drug use may lead to drug-seeking behavior that fosters continued drug use, according to the scientists.
The researchers used a microscope that allowed them to peer directly into nerve cells within the brains of living mice, and within two hours of giving a drug they found significant increases in the density of dendritic spines – structures that bear synapses required for signaling – in the animals’ frontal cortex. In contrast, mice given saline solution showed no such increase.
The researchers also found a relationship between the growth of new dendritic spines and drug-associated learning. Specifically, mice that grew the most new spines were those that developed the strongest preference for being in the enclosure where they received cocaine rather than in the enclosure where they received saline. The team published its findings online in Nature Neuroscience on August 25, 2013.
"This gives us a possible mechanism for how drug use fuels further drug-seeking behavior," said principal investigator Linda Wilbrecht, PhD, a Gallo investigator now at UC Berkeley, but who led the research while she was on the UCSF faculty.
"It’s been observed that long-term drug users show decreased function in the frontal cortex in connection with mundane cues or tasks, and increased function in response to drug-related activity or information," Wilbrecht said. "This research suggests how the brains of drug users might shift toward those drug-related associations."
In all living brains there is a baseline level of creation of new spines in response to, or in anticipation of, day-to-day learning, Wilbrecht said. By enhancing this growth, cocaine might be a super-learning stimulus that reinforces learning about the cocaine experience, she said.
The frontal cortex, which Wilbrecht called the “steering wheel” of the brain, controls functions such as long-term planning, decision-making and other behaviors involving higher reasoning and discipline.
The brain cells in the frontal cortex that Wilbrecht and her team studied regulate the output of this brain region, and may play a key role in decision-making. “These neurons, which are directly affected by cocaine use, have the potential to bias decision-making,” she said.
Wilbrecht said the findings could potentially advance research in human addiction “by helping us identify what is going awry in the frontal cortexes of drug-addicted humans, and by explaining how drug-related cues come to dominate the brain’s decision-making processes.”
In the first of a series of experiments, the scientists gave cocaine injections to one group of mice and saline injections to another. The next day, they observed the animals’ brain cells using a 2-photon laser scanning microscope. They were surprised to discover that even after the first dose, the mice treated with cocaine grew more new dendritic spines than the saline-treated mice.
In another experiment, they observed the mice before cocaine or saline treatment and then two hours afterward, and discovered that the animals that received cocaine were developing new dendritic spines within two hours after receiving the drug. Furthermore, the next morning, cocaine-induced spines accounted for almost four times more connections among nerve cells than was observed in saline-treated animals.
In a third experiment, the researchers for a week gave the mice cocaine in one distinctive chamber and saline in another, using identical procedures. Each chamber had its own characteristic visual design, texture and smell to distinguish it from the other chamber. They then let the mice choose which chamber to go to.
"The animals that showed the highest quantity of robust dendritic spines – the spines with the greatest likelihood of developing into synapses – showed the greatest change in preference toward the chamber where they received the cocaine," said Wilbrecht. "This suggests that the new spines might be material for the association that these mice have learned to make between the chamber and the drug."
Wilbrecht noted that the research would not have been possible without live brain imaging via the 2-photon laser scanning microscope, which was developed in 2002. “I grew up at the time of the famous public service campaign that showed a pan of frying eggs with the message, ‘this is your brain on drugs,’” recalled Wilbrecht. “Now, with this microscope, we can actually say, ‘this is a brain cell on drugs.’”
(Source: eurekalert.org)
How sleep helps brain learn motor task
Sleep helps the brain consolidate what we’ve learned, but scientists have struggled to determine what goes on in the brain to make that happen for different kinds of learned tasks. In a new study, researchers pinpoint the brainwave frequencies and brain region associated with sleep-enhanced learning of a sequential finger tapping task akin to typing, or playing piano.
You take your piano lesson, you go to sleep and when you wake up your fingers are better able to play that beautiful sequence of notes. How does sleep make that difference? A new study helps to explain what happens in your brain during those fateful, restful hours when motor learning takes hold.
"The mechanisms of memory consolidations regarding motor memory learning were still uncertain until now," said Masako Tamaki, a postdoctoral researcher at Brown University and lead author of the study that appears Aug. 21 in the Journal of Neuroscience. “We were trying to figure out which part of the brain is doing what during sleep, independent of what goes on during wakefulness. We were trying to figure out the specific role of sleep.”
In part because it employed three different kinds of brain scans, the research is the first to precisely quantify changes among certain brainwaves and the exact location of that changed brain activity in subjects as they slept after learning a sequential finger-tapping task. The task was a sequence of key punches that is cognitively akin to typing or playing the piano.
Specifically, the results of complex experiments performed at Massachusetts General Hospital and then analyzed at Brown show that the improved speed and accuracy volunteers showed on the task after a few hours sleep was significantly associated with changes in fast-sigma and delta brainwave oscillations in their supplementary motor area (SMA), a region on the top-middle of the brain. These specific brainwave changes in the SMA occurred during a particular phase of sleep known as “slow-wave” sleep.
Scientists have shown that sleep improves many kinds of learning, including the kind of sequential finger-tapping motor tasks addressed in the study, but they haven’t been sure about why or how. It’s an intensive activity for the brain to consolidate learning and so the brain may benefit from sleep perhaps because more energy is available or because distractions and new inputs are fewer, said study corresponding author Yuka Sasaki, a research associate professor in Brown’s Department of Cognitive, Linguistic & Psychological Sciences.
"Sleep is not just a waste of time," Sasaki said.
The extent of reorganization that the brain accomplishes during sleep is suggested by the distinct roles the two brainwave oscillations appear to play. The authors wrote that the delta oscillations appeared to govern the changes in the SMA’s connectivity with other areas of the cortex, while the fast-sigma oscillations appeared to pertain to changes within the SMA itself.
Meticulous measurements
Possible roles for fast-sigma and delta brainwaves and for the SMA had suggestive support in the literature before this study, but no one had obtained much proof in part because doing so requires a complex experimental protocol.
To make their findings, Sasaki, Tamaki and their team asked each of their 15 subjects to volunteer for the motor learning experiments. For the first three nights, nine subjects simply slept at whatever their preferred bedtime was while their brains were scanned both with magnetoencephalography (MEG), which measures the oscillations with precise timing, and polysomnography, which keeps track of sleep phase. By this time the researchers had good baseline measurements of their brain activity and subjects had become accustomed to sleeping in the lab.
On day 4, the subjects learned the finger-tapping task on their non-dominant hand (to purposely make it harder to learn). The subjects were then allowed to go to sleep for three hours and were again scanned with PSG and MEG. Then the researchers woke them up. An hour later they asked the subjects to perform the tapping task. As a control, six other subjects did not sleep after learning the task, but were also asked to perform it four hours after being trained. Those who slept did the task faster and more accurately than those who did not.
On day 5, the researchers scanned each volunteer with an magnetic resonance imaging machine, which maps brain anatomy, so that they could later see where the MEG oscillations they had observed were located in each subject’s brain.
In all, the experimenters tracked 5 different oscillation frequencies in eight brain regions (four distinct regions on each of the brain’s two sides). Sasaki said she expected the most significant activity to take place in the “M1” brain region, which governs motor control, but instead the significant changes occurred in the SMA on the opposite side of the trained hand.
What was especially important about the delta and fast-sigma oscillations was that they fit two key criteria with statistical significance: they changed substantially after subjects were trained in the task and the strength of that change correlated with the degree of the subject’s performance improvement on the task.
After performing the experiments, the team of Sasaki, Tamaki and co-author Takeo Watanabe moved from MGH to Brown, where they have set up a new sleep lab. They have since begun a project to further study how the brain consolidates learning. In this case they’re looking at visual learning tasks.
"Will we see similar effects?" Sasaki asked. "Would it be with similar frequency bands and a similar organization of neighboring brain areas?"
To find out, some volunteers will just have to sleep on it.
New clue on the origin of Huntington’s disease
The synapses in the brain act as key communication points between approximately one hundred billion neurons. They form a complex network connecting various centres in the brain through electrical impulses.
New research from Lund University suggests that it is precisely here, in the synapses, that Huntington’s disease might begin.
The researchers looked into the brains of mice with real-time imaging methods, following some of the very first stages of the disease through advanced microscopes. What they discovered was an unprecedented degradation of synaptic activity. Long before the well documented nerve cell death, synapses that are important for communication between brain centres that control memory and learning begin to wither. This process has never been mapped before and could be an important step towards understanding the serious non-motor symptoms that affect Huntington patients long before the movement disorders start to show.
“With the naked eye, we have now been able to follow the step by step events when these synapses start to break down. If we are to halt or reverse this process in the future, it is necessary to understand exactly what happens in the initial phase of the disease. Now we know more”, says Professor Jia-Yi Li, the research group leader.
Huntington’s disease has long been characterized by the involuntary writhing movements faced by patients. But in fact, Huntington’s has a very broad and highly individual symptomatology. Depression, memory loss and sleep disorders are all common early on in the disease.
“Many patients testify that these symptoms affect quality of life significantly more than the involuntary jerky movements. Therefore, it is extremely important that we achieve progress in this field of research. Our goal now is to find new therapies that can increase the lifespan of these synapses and maintain their vital function”, explains postdoc Reena, who lead the imaging experiments.
(Source: lunduniversity.lu.se)
By tracking maggots’ food choices, scientists open significant new window into human learning
The squirming larva of the humble fruit fly, which shares a surprising amount of genetic material with the human being, is helping scientists to understand the way we learn information from one another.
Fruit flies have long served as models for studying behaviour because their cognitive mechanisms are parallel to humans’, but much simpler to study.
Fruit flies exhibit many of the same basic behaviours as humans and share 87 per cent of the material that is responsible for genetically based neurological disorders, making them a potent model for study.
While adult fruit flies have been studied for decades, the new paper reveals that their larvae, which are even simpler organisms, may be more valuable models for behavioral research. A fruit fly larva has only 3,000 neurons, for example, while a human has about 10 billion.
The McMaster researchers were able to prove that the larvae, or maggots, are capable of social learning, which opens the door to many other experiments that could provide valuable insights into human behaviour, end even lead to treatments for human disorders, the scientists say.
“People have been studying adult flies for decades now,” explains the study’s lead author, Zachary Durisko. “The larval stage is much simpler in terms of the brain, but behaviour at the larval stage has been less well studied. Here we have a complex behaviour in this even simpler model.”
Durisko and Reuven Dukas, both of McMaster’s Department of Psychology, Neuroscience and Behaviour, have shown that fruit fly larvae are able to distinguish which food sources have been used by other larvae and utilize the information to benefit themselves by choosing to eat from those same established sources instead of available alternatives.
The maggots’ attraction to food that others have been eating is based on smell, and is roughly equivalent to a person arriving in a new city, seeing two restaurants and choosing a busy one over an empty one, the researchers explain.
“They prefer the social over the non-social like we would do, and they learn to prefer the social over the non-social,” Dukas says.
In fact, the motivations may be similar in each case, and could include accepting the judgment of others as an indication of quality and seeking the company of others for protection from harm.
Durisko, the lead author, recently completed his PhD at McMaster, and Dukas, his co-author, is a professor at the university. Their work is published in the prestigious Proceedings of the Royal Society B, one of the society’s biological journals.
The researchers used several combinations of foods, both completely fresh and previously used, and of varying degrees of nutritional value, to compare the maggots’ preferences.
Exercise May be the Best Medicine for Alzheimer’s
New research out of the University of Maryland School of Public Health shows that exercise may improve cognitive function in those at risk for Alzheimer’s by improving the efficiency of brain activity associated with memory. Memory loss leading to Alzheimer’s disease is one of the greatest fears among older Americans. While some memory loss is normal and to be expected as we age, a diagnosis of mild cognitive impairment, or MCI, signals more substantial memory loss and a greater risk for Alzheimer’s, for which there currently is no cure.
The study, led by Dr. J. Carson Smith, assistant professor in the Department of Kinesiology, provides new hope for those diagnosed with MCI. It is the first to show that an exercise intervention with older adults with mild cognitive impairment (average age 78) improved not only memory recall, but also brain function, as measured by functional neuroimaging (via fMRI). The findings are published in the Journal of Alzheimer’s Disease.
“We found that after 12 weeks of being on a moderate exercise program, study participants improved their neural efficiency – basically they were using fewer neural resources to perform the same memory task,” says Dr. Smith. “No study has shown that a drug can do what we showed is possible with exercise.”
Recommended Daily Activity: Good for the Body, Good for the Brain
Two groups of physically inactive older adults (ranging from 60-88 years old) were put on a 12-week exercise program that focused on regular treadmill walking and was guided by a personal trainer. Both groups – one which included adults with MCI and the other with healthy brain function – improved their cardiovascular fitness by about ten percent at the end of the intervention. More notably, both groups also improved their memory performance and showed enhanced neural efficiency while engaged in memory retrieval tasks.
The good news is that these results were achieved with a dose of exercise consistent with the physical activity recommendations for older adults. These guidelines urge moderate intensity exercise (activity that increases your heart rate and makes you sweat, but isn’t so strenuous that you can’t hold a conversation while doing it) on most days for a weekly total of 150 minutes.
Measuring Exercise’s Impact on Brain Health and Memory
One of the first observable symptoms of Alzheimer’s disease is the inability to remember familiar names. Smith and colleagues had study participants identify famous names and measured their brain activation while engaged in correctly recognizing a name – e.g., Frank Sinatra, or other celebrities well known to adults born in the 1930s and 40s. “The task gives us the ability to see what is going on in the brain when there is a correct memory performance,” Smith explains.
Tests and imaging were performed both before and after the 12-week exercise intervention. Brain scans taken after the exercise intervention showed a significant decrease in the intensity of brain activation in eleven brain regions while participants correctly identified famous names. The brain regions with improved efficiency corresponded to those involved in the pathology of Alzheimer’s disease, including the precuneus region, the temporal lobe, and the parahippocampal gyrus.
The exercise intervention was also effective in improving word recall via a “list learning task,” i.e., when people were read a list of 15 words and asked to remember and repeat as many words as possible on five consecutive attempts, and again after a distraction of being given another list of words.
“People with MCI are on a very sharp decline in their memory function, so being able to improve their recall is a very big step in the right direction,” Smith states.
The results of Smith’s study suggest that exercise may reduce the need for over-activation of the brain to correctly remember something. That is encouraging news for those who are looking for something they can do to help preserve brain function.
Dr. Smith has plans for a larger study that would include more participants, including those who are healthy but have a genetic risk for Alzheimer’s, and follow them for a longer time period with exercise in comparison to other types of treatments. He and his team hope to learn more about the impact of exercise on brain function and whether it could delay the onset or progression of Alzheimer’s disease.