Even Brief Workouts Quickly Improve Memory Function

Exercise has numerous benefits, and more and more continues to be found about how valuable consistent exercise is. Having a stronger memory will often improve performance in a variety of ways, and thus this research should give people more motivation to workout more.

People who include a little yoga or tai chi in their day may be more likely to remember where they put their keys. Researchers at the University of California, Irvine and Japan’s University of Tsukuba found that even very light workouts can increase the connectivity between parts of the brain responsible for memory formation and storage.

In a study of 36 healthy young adults, the researchers discovered that a single 10-minute period of mild exertion can yield considerable cognitive benefits. Using high-resolution functional magnetic resonance imaging, the team examined subjects’ brains shortly after exercise sessions and saw better connectivity between the hippocampal dentate gyrus and cortical areas linked to detailed memory processing.

Their results were published today in Proceedings of the National Academy of Sciences.

“The hippocampus is critical for the creation of new memories; it’s one of the first regions of the brain to deteriorate as we get older — and much more severely in Alzheimer’s disease,” said project co-leader Michael Yassa, UCI professor and Chancellor’s Fellow of neurobiology & behavior. “Improving the function of the hippocampus holds much promise for improving memory in everyday settings.”

The neuroscientists found that the level of heightened connectivity predicted the degree of recall enhancement.

Yassa, director of UCI’s Center for the Neurobiology of Learning and Memory and the recently launched UCI Brain Initiative, said that while prior research has centered on the way exercise promotes the generation of new brain cells in memory regions, this new study demonstrates a more immediate impact: strengthened communication between memory-focused parts of the brain.

“We don’t discount the possibility that new cells are being born, but that’s a process that takes a bit longer to unfold,” he said. “What we observed is that these 10-minute periods of exercise showed results immediately afterward.”

A little bit of physical activity can go a long way, Yassa stressed. “It’s encouraging to see more people keeping track of their exercise habits — by monitoring the number of steps they’re taking, for example,” he said. “Even short walking breaks throughout the day may have considerable effects on improving memory and cognition.”

Yassa and his colleagues at UCI and at the University of Tsukuba are extending this avenue of research by testing older adults who are at greater risk of age-related mental impairment and by conducting long-term interventions to see if regular, brief, light exercise done daily for several weeks or months can have a positive impact on the brain’s structure and function in these subjects.

Research: Depressive Episodes Can Damage Memory

The extent of the damage depends on the severity and length of the depressive episodes. This new research gives a concrete example of why it is important to improve mental health outcomes — it turns out that depression can have directly negative effects on the brain, and there are plenty of implications for human society based on that.

During a depressive episode the ability of the brain to form new brain cells is reduced. Scientists of the Ruhr-Universität Bochum examined how this affects the memory with a computational model. It was previously known that people in an acute depressive episode were less likely to remember current events. The computational model however suggests that older memories were affected as well. How long the memory deficits reach back depends on how long the depressive episode lasts. The team around the computational neuroscientist Prof Dr Sen Cheng published their findings in the journal PLOS ONE on 7th June 2018.

Computational model simulates a depressive brain

In major depressive disorder patients may suffer from such severe cognitive impairments that, in some cases, are called pseudodementia. Unlike in the classic form of dementia, in pseudodementia memory recovers when the depressive episode ends. To understand this process, the scientists from Bochum developed a computational model that captures the characteristic features of the brain of a patient with depressions. They tested the ability of the model to store and recall new memories.

As is the case in patients, the simulation alternated between depressive episodes and episodes without any symptoms. During a depressive episode, the brain forms fewer new neurons in the model.

Whereas in previous models, memories were represented as static patterns of neural activity, the model developed by Sen Cheng and his colleagues views memories as a sequence of neural activity patterns. “This allows us not only to store events in memory but also their temporal order,” says Sen Cheng.

Impact on brain stronger than thought

The computational model was able to recall memories more accurately, if the responsible brain region was able to form many new neurons, just like the scientists expected. However, if the brain region formed fewer new brain cells, it was harder to distinguish similar memories and to recall them separately.

The computational model not only showed deficits in recalling current events, it also struggled with memories that were collected before the depressive episode. The longer the depressive episode lasted the further the memory problems reached back.

“So far it was assumed that memory deficits only occur during a depressive episode,” says Sen Cheng. “If our model is right, major depressive disorder could have consequences that are more far reaching. Once remote memories have been damaged, they do not recover, even after the depression has subsided.”

Cognitive Impairment in Mice With Dementia Reversed

It’s a significant development for treating that disease and those similar to it.

Reversing memory deficits and impairments in spatial learning is a major goal in the field of dementia research. A lack of knowledge about cellular pathways critical to the development of dementia, however, has stood in the way of significant clinical advance. But now, researchers at the Lewis Katz School of Medicine at Temple University (LKSOM) are breaking through that barrier. They show, for the first time in an animal model, that tau pathology — the second-most important lesion in the brain in patients with Alzheimer’s disease — can be reversed by a drug.

“We show that we can intervene after disease is established and pharmacologically rescue mice that have tau-induced memory deficits,” explained senior investigator Domenico Praticò, MD, Scott Richards North Star Foundation Chair for Alzheimer’s Research, Professor in the Departments of Pharmacology and Microbiology, and Director of the Alzheimer’s Center at Temple at LKSOM. The study, published online in the journal Molecular Neurobiology, raises new hope for human patients affected by dementia.

The researchers landed on their breakthrough after discovering that inflammatory molecules known as leukotrienes are deregulated in Alzheimer’s disease and related dementias. In experiments in animals, they found that the leukotriene pathway plays an especially important role in the later stages of disease.

“At the onset of dementia, leukotrienes attempt to protect nerve cells, but over the long term, they cause damage,” Dr. Praticò said. “Having discovered this, we wanted to know whether blocking leukotrienes could reverse the damage, whether we could do something to fix memory and learning impairments in mice having already abundant tau pathology.”

[…]

After 16 weeks of treatment, animals were administered maze tests to assess their working memory and their spatial learning memory. Compared with untreated animals, tau mice that had received zileuton performed significantly better on the tests. Their superior performance suggested a successful reversal of memory deficiency.

To determine why this happened, the researchers first analyzed leukotriene levels. They found that treated tau mice experienced a 90-percent reduction in leukotrienes compared with untreated mice. In addition, levels of phosphorylated and insoluble tau, the form of the protein that is known to directly damage synapses, were 50 percent lower in treated animals. Microscopic examination revealed vast differences in synaptic integrity between the groups of mice. Whereas untreated animals had severe synaptic deterioration, the synapses of treated tau animals were indistinguishable from those of ordinary mice without the disease.

[…]

The study is especially exciting because zileuton is already approved by the Food and Drug Administration for the treatment of asthma. “Leukotrienes are in the lungs and the brain, but we now know that in addition to their functional role in asthma, they also have a functional role in dementia,” Dr. Praticò explained.

“This is an old drug for a new disease,” he added. “The research could soon be translated to the clinic, to human patients with Alzheimer’s disease.”

Memory Transferred Through Snails Using RNA Injection

Memory is one of the most important aspects of creatures with higher intelligence, and it was recently found that animals can mentally replay past events. Altering the processes that control memory could be enormously useful — as in restoring positive memories — or enormously harmful — as in deleting memories of events that were vital to learning. That’s technology’s lack of a moral imperative though — the outcome depends on how it’s used.

UCLA biologists report they have transferred a memory from one marine snail to another, creating an artificial memory, by injecting RNA from one to another. This research could lead to new ways to lessen the trauma of painful memories with RNA and to restore lost memories.

“I think in the not-too-distant future, we could potentially use RNA to ameliorate the effects of Alzheimer’s disease or post-traumatic stress disorder,” said David Glanzman, senior author of the study and a UCLA professor of integrative biology and physiology and of neurobiology. The team’s research is published May 14 in eNeuro, the online journal of the Society for Neuroscience.

RNA, or ribonucleic acid, has been widely known as a cellular messenger that makes proteins and carries out DNA’s instructions to other parts of the cell. It is now understood to have other important functions besides protein coding, including regulation of a variety of cellular processes involved in development and disease.

The researchers gave mild electric shocks to the tails of a species of marine snail called Aplysia. The snails received five tail shocks, one every 20 minutes, and then five more 24 hours later. The shocks enhance the snail’s defensive withdrawal reflex, a response it displays for protection from potential harm. When the researchers subsequently tapped the snails, they found those that had been given the shocks displayed a defensive contraction that lasted an average of 50 seconds, a simple type of learning known as “sensitization.” Those that had not been given the shocks contracted for only about one second.

The life scientists extracted RNA from the nervous systems of marine snails that received the tail shocks the day after the second series of shocks, and also from marine snails that did not receive any shocks. Then the RNA from the first (sensitized) group was injected into seven marine snails that had not received any shocks, and the RNA from the second group was injected into a control group of seven other snails that also had not received any shocks.

Remarkably, the scientists found that the seven that received the RNA from snails that were given the shocks behaved as if they themselves had received the tail shocks: They displayed a defensive contraction that lasted an average of about 40 seconds.

[…]

Scientists know more about the cell biology of this simple form of learning in this animal than any other form of learning in any other organism, Glanzman said. The cellular and molecular processes seem to be very similar between the marine snail and humans, even though the snail has about 20,000 neurons in its central nervous system and humans are thought to have about 100 billion.

In the future, Glanzman said, it is possible that RNA can be used to awaken and restore memories that have gone dormant in the early stages of Alzheimer’s disease. He and his colleagues published research in the journal eLife in 2014 indicating that lost memories can be restored.

First Evidence that Animals Can Mentally Replay Past Events Found

Many innovations and breakthroughs have been based on or inspired by better understandings of animals, such as understanding bats leading to sonar and understanding scorpion venom leading to the development of new medicines. Perhaps animals have different mental processes than humans to remember past events, but in any case, there’s likely benefits to this research still unseen.

Neuroscientists at Indiana University have reported the first evidence that non-human animals can mentally replay past events from memory. The discovery could help advance the development of new drugs to treat Alzheimer’s disease.

The study, led by IU professor Jonathon Crystal, appears today in the journal Current Biology.

“The reason we’re interested in animal memory isn’t only to understand animals, but rather to develop new models of memory that match up with the types of memory impaired in human diseases such as Alzheimer’s disease,” said Crystal, a professor in the IU Bloomington College of Arts and Sciences’ Department of Psychological and Brain Sciences and director of the IU Bloomington Program in Neuroscience.

Under the current paradigm, Crystal said most preclinical studies on potential new Alzheimer’s drugs examine how these compounds affect spatial memory, one of the easiest types of memory to assess in animals. But spatial memory is not the type of memory whose loss causes the most debilitating effects of Alzheimer’s disease.

“If your grandmother is suffering from Alzheimer’s, one of the most heartbreaking aspects of the disease is that she can’t remember what you told her about what’s happening in your life the last time you saw her,” said Danielle Panoz-Brown, an IU Ph.D. student who is the first author on the study. “We’re interested in episodic memory — and episodic memory replay — because it declines in Alzheimer’s disease, and in aging in general.”

Episodic memory is the ability to remember specific events. For example, if a person loses their car keys, they might try to recall every single step — or “episode” — in their trip from the car to their current location. The ability to replay these events in order is known as “episodic memory replay.” People wouldn’t be able to make sense of most scenarios if they couldn’t remember the order in which they occurred, Crystal said.

To assess animals’ ability to replay past events from memory, Crystal’s lab spent nearly a year working with 13 rats, which they trained to memorize a list of up to 12 different odors. The rats were placed inside an “arena” with different odors and rewarded when they identified the second-to-last odor or fourth-to-last odor in the list.

The team changed the number of odors in the list prior to each test to confirm the odors were identified based upon their position in the list, not by scent alone, proving the animals were relying on their ability to recall the whole list in order. Arenas with different patterns were used to communicate to the rats which of the two options was sought.

After their training, Crystal said, the animals successfully completed their task about 87 percent of the time across all trials. The results are strong evidence the animals were employing episodic memory replay.

Additional experiments confirmed the rats’ memories were long-lasting and resistant to “interference” from other memories, both hallmarks of episodic memory. They also ran tests that temporarily suppressed activity in the hippocampus — the site of episodic memory — to confirm the rats were using this part of their brain to perform their tasks.

Crystal said the need to find reliable ways to test episodic memory replay in rats is urgent since new genetic tools are enabling scientists to create rats with neurological conditions similar to Alzheimer’s disease. Until recently, only mice were available with the genetic modifications needed to study the effect of new drugs on these symptoms.

“We’re really trying push the boundaries of animal models of memory to something that’s increasingly similar to how these memories work in people,” he said. “If we want to eliminate Alzheimer’s disease, we really need to make sure we’re trying to protect the right type of memory.”

Prosthetic Human Memory System Implant Successful

It’s shown to boost memory, but the fact of the software-based neural implant being demonstrated seems like it’ll have significant future implications in other ways too.

Scientists at Wake Forest Baptist Medical Center and the University of Southern California (USC) have demonstrated the successful implementation of a prosthetic system that uses a person’s own memory patterns to facilitate the brain’s ability to encode and recall memory.

In the pilot study, published in today’s Journal of Neural Engineering, participants’ short-term memory performance showed a 35 to 37 percent improvement over baseline measurements.

“This is the first time scientists have been able to identify a patient’s own brain cell code or pattern for memory and, in essence, ‘write in’ that code to make existing memory work better, an important first step in potentially restoring memory loss,” said the study’s lead author Robert Hampson, Ph.D., professor of physiology/pharmacology and neurology at Wake Forest Baptist.

The study focused on improving episodic memory, which is the most common type of memory loss in people with Alzheimer’s disease, stroke and head injury. Episodic memory is information that is new and useful for a short period of time, such as where you parked your car on any given day. Reference memory is information that is held and used for a long time, such as what is learned in school.

The researchers enrolled epilepsy patients at Wake Forest Baptist who were participating in a diagnostic brain-mapping procedure that used surgically implanted electrodes placed in various parts of the brain to pinpoint the origin of the patients’ seizures. Using the team’s electronic prosthetic system based on a multi-input multi-output (MIMO) nonlinear mathematical model, the researchers influenced the firing patterns of multiple neurons in the hippocampus, a part of the brain involved in making new memories in eight of those patients.

First, they recorded the neural patterns or ‘codes’ while the study participants were performing a computerized memory task. The patients were shown a simple image, such as a color block, and after a brief delay where the screen was blanked, were then asked to identify the initial image out of four or five on the screen.

[…]

“We showed that we could tap into a patient’s own memory content, reinforce it and feed it back to the patient,” Hampson said. “Even when a person’s memory is impaired, it is possible to identify the neural firing patterns that indicate correct memory formation and separate them from the patterns that are incorrect. We can then feed in the correct patterns to assist the patient’s brain in accurately forming new memories, not as a replacement for innate memory function, but as a boost to it.

“To date we’ve been trying to determine whether we can improve the memory skill people still have. In the future, we hope to be able to help people hold onto specific memories, such as where they live or what their grandkids look like, when their overall memory begins to fail.”

Too Much Time in Dimly Lit Rooms May Decrease Intelligence, Neuroscience Research Finds

There’s a lot that could be said about this and the structural effects from it.

Spending too much time in dimly lit rooms and offices may actually change the brain’s structure and hurt one’s ability to remember and learn, indicates groundbreaking research by Michigan State University neuroscientists.

The researchers studied the brains of Nile grass rats (which, like humans, are diurnal and sleep at night) after exposing them to dim and bright light for four weeks. The rodents exposed to dim light lost about 30 percent of capacity in the hippocampus, a critical brain region for learning and memory, and performed poorly on a spatial task they had trained on previously.

The rats exposed to bright light, on the other hand, showed significant improvement on the spatial task. Further, when the rodents that had been exposed to dim light were then exposed to bright light for four weeks (after a month-long break), their brain capacity — and performance on the task — recovered fully.

The study, funded by the National Institutes of Health, is the first to show that changes in environmental light, in a range normally experienced by humans, leads to structural changes in the brain. Americans, on average, spend about 90 percent of their time indoors, according to the Environmental Protection Agency.

“When we exposed the rats to dim light, mimicking the cloudy days of Midwestern winters or typical indoor lighting, the animals showed impairments in spatial learning,” said Antonio “Tony” Nunez, psychology professor and co-investigator on the study. “This is similar to when people can’t find their way back to their cars in a busy parking lot after spending a few hours in a shopping mall or movie theater.”

Nunez collaborated with Lily Yan, associate professor of psychology and principal investigator on the project, and Joel Soler, a doctoral graduate student in psychology. Soler is also lead author of a paper on the findings published in the journal Hippocampus.

Soler said sustained exposure to dim light led to significant reductions in a substance called brain derived neurotrophic factor — a peptide that helps maintain healthy connections and neurons in the hippocampus — and in dendritic spines, or the connections that allow neurons to “talk” to one another.

“Since there are fewer connections being made, this results in diminished learning and memory performance that is dependent upon the hippocampus,” Soler said.

[…]

The project could have implications for the elderly and people with glaucoma, retinal degeneration or cognitive impairments.

“For people with eye disease who don’t receive much light, can we directly manipulate this group of neurons in the brain, bypassing the eye, and provide them with the same benefits of bright light exposure?” Yan said. “Another possibility is improving the cognitive function in the aging population and those with neurological disorders. Can we help them recover from the impairment or prevent further decline?”