NS/ Brain waves driven by remembering events identified
Neuroscience biweekly vol. 90, 19th July — 2nd August
TL;DR
- Neurons produce rhythmic patterns of electrical activity in the brain. One of the unsettled questions in the field of neuroscience is what primarily drives these rhythmic signals, called oscillations. University of Arizona researchers have found that simply remembering events can trigger them, even more so than when people are experiencing the actual event.
- What makes the vital layer of protective cells around the brain and spinal cord — the blood-brain barrier — more or less permeable has been one of the more mystifying questions in neuroscience. Understanding how the barrier works to allow in or keep out certain substances has critical implications for everything from disease progression to drug delivery. Now, a new Harvard Medical School study, published in Developmental Cell, has brought scientists a step closer to figuring it out.
- Boosting the activity of inhibitory interneurons in Fragile X mice reduced their hypersensitivity to sensory stimuli, according to a new Neuron study led by UCLA Health researchers.
- Averting our eyes from things that scare us may be due to a specific cluster of neurons in a visual region of the brain, according to new research. Researchers found that in fruit fly brains, these neurons release a chemical called tachykinin which appears to control the fly’s movement to avoid facing a potential threat. Fruit fly brains can offer a useful analogy for larger mammals, so this research may help us better understand our own human reactions to scary situations and phobias. Next, the team wants to find out how these neurons fit into the wider circuitry of the brain so they can ultimately map out how fear controls vision.
- Researchers developed a method to produce artificially grown miniature brains — called human brain organoids — free of animal cells that could greatly improve the way neurodegenerative conditions are studied and, eventually, treated. The work offers a solution to overcome Matrigel’s weaknesses.
- A new study by a Virginia Commonwealth University researcher has found that aggression is not always the product of poor self-control but, instead, often can be the product of successful self-control in order to inflict greater retribution.
- That experiences leave their trace in the connectivity of the brain has been known for a while, but a pioneering study now shows how massive these effects really are. The findings in mice provide unprecedented insights into the complexity of large-scale neural networks and brain plasticity. Moreover, they could pave the way for new brain-inspired artificial intelligence methods.
- Being smart pays off, as it allows for more balanced decision-making. However, the origins of these abilities during evolution remain largely unexplored. Only if smarter individuals enjoy better survival and have higher reproductive rates than their conspecifics, improved cognitive abilities can evolve. Researchers from the German Primate Center (DPZ) — Leibniz Institute for Primate Research have recently examined the link between cognitive abilities and survival in gray mouse lemurs. The study involved capturing the animals, subjecting them to various cognition and personality tests, measuring their weight, and subsequently releasing them. The findings revealed that the animals that performed best in the cognition tests lived for longer. Additionally, those that were heavier and displayed more exploratory behavior also experienced an increased lifespan.
- ‘Metarecognition’ is the ability to objectively monitor, control, and improve one’s learning ability. Researchers demonstrated that the human brain exhibits metacognitive abilities that regulate implicit motor learning to maximize monetary rewards. Unlike artificial intelligence, which is perpetually optimal, human metacognition exhibits an asymmetric bias in managing rewards (monetary gain) and punishments (monetary loss).
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Memory-related processing is the primary driver of human hippocampal theta oscillations
by Sarah E. Seger, Jennifer L.S. Kriegel, Brad C. Lega, Arne D. Ekstrom in Neuron
Neurons produce rhythmic patterns of electrical activity in the brain. One of the unsettled questions in the field of neuroscience is what primarily drives these rhythmic signals, called oscillations. University of Arizona researchers have found that simply remembering events can trigger them, even more so than when people are experiencing the actual event.
The researchers specifically focused on what are known as theta oscillations, which emerge in the brain’s hippocampus region during activities like exploration, navigation and sleep. The hippocampus plays a crucial role in the brain’s ability to remember the past.
Prior to this study, it was believed that the external environment played a more important role in driving theta oscillations, said Arne Ekstrom, professor of cognition and neural systems at the UArizona Department of Psychology and senior author of the study. But Ekstrom and his collaborators found that memory generated in the brain is the main driver of theta activity.
“Surprisingly, we found that theta oscillations in humans are more prevalent when someone is just remembering things, compared to experiencing events directly,” said lead study author Sarah Seger, a graduate student in the Department of Neuroscience.
The results of the study could have implications for treating patients with brain damage and cognitive impairments, including patients who have experienced seizures, stroke and Parkinson’s disease, Ekstrom said. Memory could be used to create stimulations from within the brain and drive theta oscillations, which could potentially lead to improvements in memory over time, he said.
UArizona researchers collaborated on the study with researchers from the University of Texas Southwestern Medical Center in Dallas, including neurosurgeon Dr. Brad Lega and research technician Jennifer Kriegel. The researchers recruited 13 patients who were being monitored at the center in preparation for epilepsy surgery. As part of the monitoring, electrodes were implanted in the patients’ brains for detecting occasional seizures. The researchers recorded the theta oscillations in the hippocampus of the brain.
The patients participated in a virtual reality experiment, in which they were given a joystick to navigate to shops in a virtual city on a computer. When they arrived at the correct destination, the virtual reality experiment was paused. The researchers asked the participants to imagine the location at which they started their navigation and instructed them to mentally navigate the route they just passed through. The researchers then compared theta oscillations during initial navigation to participants’ subsequent recollection of the route.
During the actual navigation process using the joystick, the oscillations were less frequent and shorter in duration compared to oscillations that occurred when participants were just imagining the route. So, the researchers conclude that memory is a strong driver of theta oscillations in humans.
One way to compensate for impaired cognitive function is by using cognitive training and rehabilitation, Ekstrom said.
“Basically, you take a patient who has memory impairments, and you try to teach them to be better at memory,” he said.
In the future, Ekstrom is planning to conduct this research in freely walking patients as opposed to patients in beds and find how freely navigating compares to memory with regard to brain oscillations.
“Being able to directly compare the oscillations that were present during the original experience, and during a later retrieval of that is a huge step forward in the field in terms of designing new experiments and understanding the neural basis of memory,” Seger said.
The secreted neuronal signal spock1 promotes blood-brain barrier development
by Natasha M. O’Brown, Nikit B. Patel, Ursula Hartmann, Allon M. Klein, Chenghua Gu, Sean G. Megason in Developmental Cell
What makes the vital layer of protective cells around the brain and spinal cord — the blood-brain barrier — more or less permeable has been one of the more mystifying questions in neuroscience. Understanding how the barrier works to allow in or keep out certain substances has critical implications for everything from disease progression to drug delivery. Now, a new Harvard Medical School study, published in Developmental Cell, has brought scientists a step closer to figuring it out.
Working in zebrafish and mice, the team discovered that a signal originating from a gene in neurons is essential for the proper formation of the blood-brain barrier during embryonic development and helps ensure that the barrier remains intact throughout adulthood.
If replicated in further animal testing and eventually in humans, the findings could help scientists control the permeability of the blood-brain barrier. In doing so, researchers may be able to develop more effective ways of delivering cancer or psychiatric medicines into the brain and better strategies for combating barrier damage caused by neurodegeneration or stroke.
The blood-brain barrier is made of tightly interlaced cells — endothelial cells, pericytes, and astrocytes — lining the blood vessels of the brain and spinal cord that make up the central nervous system. Together, these cells form a layered, semipermeable membrane that selectively lets in nutrients and small molecules, while keeping out harmful substances.
“In normal, day-to-day life, you need a blood-brain barrier to help protect you from invading toxins and pathogens in the blood,” explained lead author Natasha O’Brown, a research fellow in systems biology at HMS who is starting her lab at Rutgers University in September.
In the case of neurodegenerative diseases such as Alzheimer’s or Parkinson’s, or stroke, the barrier begins to break down, leaving the central nervous system susceptible to infection. On the flip side, the impermeability of the barrier presents an obstacle to delivering drugs to the brain.
For decades, scientists have known that the permeability of the blood-brain barrier is in part controlled by cells in the surrounding environment — known as the microenvironment. However, the genes in those nearby cells have largely remained a mystery.
Unbeknownst to the researchers, a major clue was swimming around inside fish tanks in the lab of senior author Sean Megason, professor of systems biology in the Blavatnik Institute at HMS.
O’Brown was studying a gene called mfsd2aa that, when mutated, causes the blood-brain barrier in zebrafish to become leaky throughout the entire brain. However, she noticed that some zebrafish had a barrier that was permeable in the forebrain and midbrain, but intact in the hindbrain.
“This observation led me down a rabbit hole of finding the gene that causes the blood-brain barrier to become regionally permeable,” she said.
O’Brown conducted genetic screens on the zebrafish and discovered that the region-specific breakdown of the barrier was linked to a mutation in spock1 — a gene whose name brought to mind the Star Trek character but was otherwise unfamiliar to her.
In a series of experiments in zebrafish and mice, O’Brown confirmed that a spock1 mutation caused the blood-brain barrier to become permeable in some areas but not others. She also saw that spock1 was expressed in neurons throughout the retina, brain, and spinal cord, but not in the cells that make up the barrier itself.
In follow-up experiments, animals with a spock1 mutation had more vesicles — intercellular bubbles that can carry large molecules across the blood-brain barrier — in their endothelial cells. They also had a smaller basement membrane, a network of proteins found between endothelial cells and pericytes in the barrier. Cell-by-cell RNA analysis revealed that spock1 caused changes in gene expression in endothelial cells and pericytes in the blood-brain barrier, but not in other cell types in the brain. When O’Brown injected a dose ofhuman SPOCK1protein into zebrafish brains, it restored around 50 percent of blood-brain barrier function by repairing pericyte-endothelial cell interactions at a molecular level.
Based on these findings, the researchers concluded that the Spock1protein produced by neurons travels to the blood-brain barrier, where it initiates the proper formation of the barrier during development and helps maintain the barrier after.
“Spock1 is a potent secreted neural signal that is able to promote and induce barrier properties in these blood vessels; without it, you don’t get a functional blood-brain barrier,” O’Brown said. “It’s like a spark on a gas stove, providing a cue that tells the barrier program to turn on.”
The study adds to a growing body of research by blood-brain barrier biologist Chenghua Gu, professor of neurobiology at HMS, investigator at the Howard Hughes Medical Institute, and an author of the new paper. Her lab has been studying a cellular trafficking system that seems to regulate blood-brain barrier permeability through Mfsd2a, and exploring other aspects of the microenvironment that may be involved. Cumulatively, the work is providing scientists with an increasingly complete picture of how the blood-brain barrier functions.
Gaining this complete picture is essential as researchers attempt to manipulate the permeability of the barrier. For drug delivery, they often want to make the barrier more permeable, so therapies known to be effective for cancer or psychiatric disorders can reach the brain and do their jobs. For neurodegenerative diseases such as Parkinson’s and Alzheimer’s or situations like stroke, scientists want to counter the associated deterioration of the blood-brain barrier that makes the central nervous system vulnerable to external assaults.
O’Brown noted that spock1 is an especially appealing target for controlling the properties of the blood-brain barrier because it is conserved in humans and seems to act as a high-level regulator of barrier cells during development.
She now wants to explore how different lineages of pericytes in the barrier are differentially affected by spock1 signaling. She would also like to test out stroke models, to see if administering spock1 can counter a stroke’s effects on the blood-brain barrier.
“This isn’t the first neural signal scientists have found, but it is the first signal from neurons that specifically seems to regulate barrier properties,” O’Brown said. “I think this makes it a potent tool to try and toggle the switch.”
Improvement of sensory deficits in fragile X mice by increasing cortical interneuron activity after the critical period
by Nazim Kourdougli, Anand Suresh, Benjamin Liu, Pablo Juarez, Ashley Lin, David T. Chung, Anette Graven Sams, Michael J. Gandal, Verónica Martínez-Cerdeño, Dean V. Buonomano, Benjamin J. Hall, Cédric Mombereau, Carlos Portera-Cailliau in Neuron
Boosting the activity of inhibitory interneurons in Fragile X mice reduced their hypersensitivity to sensory stimuli, according to a new Neuron study led by UCLA Health researchers.
Fragile X Syndrome, which is caused by a mutation in a single gene, is the most common inherited form of intellectual disability and autism. Many people with Fragile X are extremely sensitive to sights, sounds, and touch, among other sensory experiences.
Previous research found Fragile X mice have a lower density of parvalbumin (PV) inhibitory interneurons, the main class of inhibitory neurons in the cerebral cortex — the region of the brain responsible for sensory processing. These neurons act like a brake on excitatory neurons to help them fire only when necessary.
Because autism symptoms first appear during the toddler stage and likely reflect changes in the brain that happened earlier, the researchers sought to establish when the reduced activity of PV interneurons was first apparent during brain development in mice — and whether the intervention could help mitigate sensory hypersensitivity.
Researchers recorded neuronal activity in the brains of young mice during the first two weeks of life. They then sought to influence this activity through a novel drug compound that boosts the firing of PV neurons.
Researchers found that the density of PV neurons is indeed lower in Fragile X mice compared to controls — but even in mice as young as six days old. There were also greater numbers of dying PV neurons during early development in Fragile X mice, suggesting that these neurons are dying at a higher rate than what is considered healthy.
They also found that PV neurons in young Fragile X mice were unable to regulate the activity of excitatory neurons during the first two weeks of development, indicating that these neurons are functionally decoupled during this time. That could explain why researchers were able to restore PV neuron density by boosting PV neuron activity during this period of development but could not restore the activity of excitatory neurons.
Researchers then administered a novel drug compound aimed at activating PV neurons in Fragile X mice during the third week of development. The treatment restored the ability of excitatory neurons to respond to touch, resembling how they function in healthy controls. It also reduced hypersensitivity to repeated touch, which is similar to what is known as tactile defensiveness in humans with Fragile X.
While there are no existing treatments for the root cause of Fragile X, there are medications that address symptoms like anxiety, ADHD, or seizures. The new research suggests modulating the activity of PV neurons could be an effective approach to restoring circuit function.
“Our research is an example of how therapies that target circuit differences in neurodevelopmental conditions, like boosting the activity of inhibitory neurons in the brain, could help mitigate bothersome symptoms such as sensory hypersensitivity,” said corresponding author Carlos Portera-Cailliau, MD, PhD, a professor of neurology and neurobiology at the David Geffen School of Medicine at UCLA. Nazim Kourdougli, PhD, a postdoctoral fellow in Portera-Cailliau’s lab, is the first author.
Portera-Cailliau’s lab will continue investigating how inhibitory neurons make synapses with excitatory neurons during development, and how the mutation in Fragile X affects this process. It will also test if the same drug compound can ameliorate other behavioral differences in Fragile X mice.
Threat gates visual aversion via theta activity in Tachykinergic neurons
by Masato Tsuji, Yuto Nishizuka, Kazuo Emoto in Nature Communications
Averting our eyes from things that scare us may be due to a specific cluster of neurons in a visual region of the brain, according to new research at the University of Tokyo. Researchers found that in fruit fly brains, these neurons release a chemical called tachykinin which appears to control the fly’s movement to avoid facing a potential threat. Fruit fly brains can offer a useful analogy for larger mammals, so this research may help us better understand our own human reactions to scary situations and phobias. Next, the team want to find out how these neurons fit into the wider circuitry of the brain so they can ultimately map out how fear controls vision.
Do you cover your eyes during horror movies? Or perhaps the sight of a spider makes you turn and run? Avoiding looking at things that scare us is a common experience, for humans and animals. But what actually makes us avert our gaze from the things we fear? Researchers have found that it may be due to a group of neurons in the brain that regulates vision when feeling afraid.
“We discovered a neuronal mechanism by which fear regulates visual aversion in the brains of Drosophila (fruit flies). It appears that a single cluster of 20–30 neurons regulates vision when in a state of fear. Since fear affects vision across animal species, including humans, the mechanism we found may be active in humans as well,” explained Assistant Professor Masato Tsuji from the Department of Biological Sciences at the University of Tokyo.
The team used puffs of air to simulate a physical threat and found that the flies’ walking speed increased after being puffed at. The flies also would choose a puff-free route if offered, showing that they perceived the puffs as a threat (or at least preferred to avoid them). Next, the researchers placed a small black object, roughly the size of a spider, 60 degrees to the right or left of the fly. On its own, the object didn’t cause a change in behavior, but when placed following puffs of air, the flies avoided looking at the object and moved so that it was positioned behind them.
To understand the molecular mechanism underlying this aversion behavior, the team then used mutated flies in which they altered the activity of certain neurons. While the mutated flies kept their visual and motor functions, and would still avoid the air puffs, they did not respond in the same fearful manner to visually avoid the object.
“This suggested that the cluster of neurons which releases the chemical tachykinin was necessary for activating visual aversion,” said Tsuji. “When monitoring the flies’ neuronal activity, we were surprised to find that it occurred through an oscillatory pattern, i.e., the activity went up and down similar to a wave. Neurons typically function by just increasing their activity levels, and reports of oscillating activity are particularly rare in fruit flies because up until recently the technology to detect this at such a small and fast scale didn’t exist.”
By giving the flies genetically encoded calcium indicators, the researchers could make the flies’ neurons shine brightly when activated. Thanks to the latest imaging techniques, they then saw the changing, wavelike pattern of light being emitted, which was previously averaged out and missed.
Next, the team wants to figure out how these neurons fit into the broader circuitry of the brain. Although the neurons exist in a known visual region of the brain, the researchers do not yet know from where the neurons are receiving inputs and to where they are transmitting them, to regulate visual escape from objects perceived as dangerous.
“Our next goal is to uncover how visual information is transmitted within the brain, so that we can ultimately draw a complete circuit diagram of how fear regulates vision,” said Tsuji. “One day, our discovery might perhaps provide a clue to help with the treatment of psychiatric disorders stemming from exaggerated fear, such as anxiety disorders and phobias.”
Engineered extracellular matrices facilitate brain organoids from human pluripotent stem cells
by Ayşe J. Muñiz, Tuğba Topal, Michael D. Brooks, Angela Sze, Do Hoon Kim, Jacob Jordahl, Joe Nguyen, Paul H. Krebsbach, Masha G. Savelieff, Eva L. Feldman, Joerg Lahann in Annals of Clinical and Translational Neurology
Researchers at the University of Michigan developed a method to produce artificially grown miniature brains — called human brain organoids — free of animal cells that could greatly improve the way neurodegenerative conditions are studied and, eventually, treated.
Over the last decade of researching neurologic diseases, scientists have explored the use of human brain organoids as an alternative to mouse models. These self-assembled, 3D tissues derived from embryonic or pluripotent stem cells more closely model the complex brain structure compared to conventional two-dimensional cultures.
Until now, the engineered network of proteins and molecules that give structure to the cells in brain organoids, known as extracellular matrices, often used a substance derived from mouse sarcomas called Matrigel. That method suffers significant disadvantages, with a relatively undefined composition and batch-to-batch variability.
The latest U-M research, published in Annals of Clinical and Translational Neurology, offers a solution to overcome Matrigel’s weaknesses. Investigators created a novel culture method that uses an engineered extracellular matrix for human brain organoids — without the presence of animal components — and enhanced the neurogenesis of brain organoids compared to previous studies.
“This advancement in the development of human brain organoids free of animal components will allow for significant strides in the understanding of neurodevelopmental biology,” said senior author Joerg Lahann, Ph.D., director of the U-M Biointerfaces Institute and Wolfgang Pauli Collegiate Professor of Chemical Engineering at U-M.
“Scientists have long struggled to translate animal research into the clinical world, and this novel method will make it easier for translational research to make its way from the lab to the clinic.”
The foundational extracellular matrices of the research team’s brain organoids were composed of human fibronectin, a protein that serves as a native structure for stem cells to adhere, differentiate and mature. They were supported by a highly porous polymer scaffold.
The organoids were cultured for months, while lab staff was unable to enter the building due to the COVID 19-pandemic.
Using proteomics, researchers found their brain organoids developed cerebral spinal fluid, a clear liquid that flows around healthy brain and spinal cords. This fluid more closely matched human adult CSF compared to a landmark study of human brain organoids developed in Matrigel.
“When our brains are naturally developing in utero, they are of course not growing on a bed of extracellular matrix produced by mouse cancer cells,” said first author Ayse Muñiz, Ph.D., who was a graduate student in the U-M Macromolecular Science and Engineering Program at the time of the work.
“By putting cells in an engineered niche that more closely resembles their natural environment, we predicted we would observe differences in organoid development that more faithfully mimics what we see in nature.”
The success of these xenogeneic-free human brain organoids opens the door for reprogramming cells from patients with neurodegenerative diseases, says co-author Eva Feldman, M.D., Ph.D., director of the ALS Center of Excellence at U-M and James W. Albers Distinguished Professor of Neurology at U-M Medical School.
“There is a possibility to take the stem cells from a patient with a condition such as ALS or Alzheimer’s and, essentially, build an avatar mini brain of that patients to investigate possible treatments or model how their disease will progress,” Feldman said. “These models would create another avenue to predict disease and study treatment on a personalized level for conditions that often vary greatly from person to person.”
Aggression as successful self‐control
by David S. Chester in Social and Personality Psychology Compass
A new study by a Virginia Commonwealth University researcher has found that aggression is not always the product of poor self-control but, instead, often can be the product of successful self-control in order to inflict greater retribution.
The paper by corresponding author David Chester, Ph.D., an associate professor of social psychology in the Department of Psychology at VCU’s College of Humanities and Sciences, was published by the journal Social and Personality Psychology Compass and uses meta-analysis to summarize evidence from dozens of existing studies in psychology and neurology.
“Typically, people explain violence as the product of poor self-control,” Chester said. “In the heat of the moment, we often fail to inhibit our worst, most aggressive impulses. But that is only one side of the story.”
Indeed, Chester’s study found that the most aggressive people do not have personalities characterized by poor self-discipline and that training programs that boost self-control have not proved effective in reducing violent tendencies. Instead, the study found ample evidence that aggression can arise from successful self-control.
“Vengeful people tend to exhibit greater premeditation of their behavior and self-control, enabling them to delay the gratification of sweet revenge and bide their time to inflict maximum retribution upon those who they believe have wronged them,” Chester said. “Even psychopathic people, who comprise the majority of people who commit violent offenses, often exhibit robust development of inhibitory self-control over their teenage years.”
Aggressive behavior is reliably linked to increased — not just decreased — activity in the brain’s prefrontal cortex, a biological substrate of self-control, Chester found. The findings make it clear that the argument that aggression is primarily the product of poor self-control is weaker than previously thought.
“This paper pushes back against a decades-long dominant narrative in aggression research, which is that violence starts when self-control stops,” Chester said. “Instead, it argues for a more balanced, nuanced view in which self-control can both constrain and facilitate aggression, depending on the person and the situation.”
The findings also argue for more caution in the implementation of treatments, therapies and interventions that seek to reduce violence by improving self-control, Chester said.
“Many interventions seek to teach people to inhibit their impulses, but this new approach to aggression suggests that although this may reduce aggression for some people, it is also likely to increase aggression for others,” he said. “Indeed, we may be teaching some people how best to implement their aggressive tendencies.”
The findings surprised Chester, a psychologist whose team frequently studies the causes of human aggression.
“Over the years, much of our research was guided by the field’s assumption that aggression is an impulsive behavior characterized by poor self-control,” he said. “But as we started to investigate the psychological characteristics of vengeful and psychopathic people, we quickly realized that such aggressive individuals do not just have self-regulatory deficits; they have many psychological adaptations and skills that enable them to hurt others by using self-control.”
Chester and his team plan to continue exploring questions around aggression and self-control based on the study’s findings.
“Our research going forward is now guided by this new paradigm shift in thinking: that aggression is often the product of sophisticated and complex mental processes and not just uninhibited impulses,” Chester said.
High-resolution CMOS-based biosensor for assessing hippocampal circuit dynamics in experience-dependent plasticity
by Brett Addison Emery, Xin Hu, Shahrukh Khanzada, Gerd Kempermann, Hayder Amin in Biosensors and Bioelectronics
That experiences leave their trace in the connectivity of the brain has been known for a while, but a pioneering study by researchers at the German Center for Neurodegenerative Diseases (DZNE) and TUD Dresden University of Technology now shows how massive these effects really are. The findings in mice provide unprecedented insights into the complexity of large-scale neural networks and brain plasticity. Moreover, they could pave the way for new brain-inspired artificial intelligence methods. The results, based on an innovative “brain-on-chip” technology, are published in the scientific journal Biosensors and Bioelectronics.
The Dresden researchers explored the question of how an enriched experience affects the brain’s circuitry. For this, they deployed a so-called neurochip with more than 4,000 electrodes to detect the electrical activity of brain cells. This innovative platform enabled registering the “firing” of thousands of neurons simultaneously. The area examined — much smaller than the size of a human fingernail — covered an entire mouse hippocampus. This brain structure, shared by humans, plays a pivotal role in learning and memory, making it a prime target for the ravages of dementias like Alzheimer’s disease. For their study, the scientists compared brain tissue from mice, which were raised differently. While one group of rodents grew up in standard cages, which did not offer any special stimuli, the others were housed in an “enriched environment” that included rearrangeable toys and maze-like plastic tubes.
“The results by far exceeded our expectations,” said Dr. Hayder Amin, lead scientist of the study. Amin, a neuroelectronics and nomputational neuroscience expert, heads a research group at DZNE. With his team, he developed the technology and analysis tools used in this study. “Simplified, one can say that the neurons of mice from the enriched environment were much more interconnected than those raised in standard housing. No matter which parameter we looked at, a richer experience literally boosted connections in the neuronal networks. These findings suggest that leading an active and varied life shapes the brain on whole new grounds.”
Prof. Gerd Kempermann, who co-leads the study and has been working on the question of how physical and cognitive activity helps the brain to form resilience towards aging and neurodegenerative disease, attests:
“All we knew in this area so far has either been taken from studies with single electrodes or imaging techniques like magnetic resonance imaging. The spatial and temporal resolution of these techniques is much coarser than our approach. Here we can literally see the circuitry at work down to the scale of single cells. We applied advanced computational tools to extract a huge amount of details about network dynamics in space and time from our recordings.”
“We have uncovered a wealth of data that illustrates the benefits of a brain shaped by rich experience. This paves the way to understand the role of plasticity and reserve formation in combating neurodegenerative diseases, especially with respect to novel preventive strategies,” Prof. Kempermann said, who, in addition to being a DZNE researcher, is also affiliated with the Center for Regenerative Therapies Dresden (CRTD) at TU Dresden. “Also, this will help provide insights into disease processes associated with neurodegeneration, such as dysfunctions of brain networks.”
“By unraveling how experiences shape the brain’s connectome and dynamics, we are not only pushing the boundaries of brain research,” states Dr. Amin. “Artificial intelligence is inspired by how the brain computes information. Thus, our tools and the insights they allow to generate could open the way for novel machine learning algorithms.”
Cognitive performance is linked to fitness in a wild primate
by Claudia Fichtel, Johanna Henke-von der Malsburg, Peter M. Kappeler in Science Advances
Being smart pays off, as it allows for more balanced decision-making. However, the origins of these abilities during evolution remain largely unexplored. Only if smarter individuals enjoy better survival and have higher reproductive rates than their conspecifics, improved cognitive abilities can evolve. Researchers from the German Primate Center (DPZ) — Leibniz Institute for Primate Research have recently examined the link between cognitive abilities and survival in gray mouse lemurs.
The study involved capturing the animals, subjecting them to various cognition and personality tests, measuring their weight, and subsequently releasing them. The findings revealed that the animals that performed best in the cognition tests lived for longer. Additionally, those that were heavier and displayed more exploratory behavior also experienced an increased lifespan. These results suggest that alternative strategies can contribute to an extended lifespan (Science Advances).
Cognitive abilities not only vary among different species but also among individuals within the same species. It is expected that smarter individuals live longer, as they are likely to make better decisions, regarding habitat and food selection, predator avoidance, and infant care. To investigate the factors influencing the life expectancy of wild gray mouse lemurs, researchers from the German Primate Center conducted a long-term study in Madagascar.
They administered four different cognitive tests and two personality tests to 198 animals, while also measuring their weight and tracking their survival over several years. The cognition tests assessed problem-solving (reaching food by manipulating a slider), spatial memory (remembering the location of hidden food), inhibitory control (taking a detour to access food), and causal understanding (retrieving food by pulling a string). The first personality test evaluated exploratory behavior, while the second measured curiosity through the animals’ reactions to unfamiliar objects.
In the study, individuals that performed better in the cognitive tests exhibited less exploratory behavior compared to poorer-performing conspecifics. Conversely, more explorative individuals had higher weights, likely due to their ability to find food more easily. The study also found that animals with better cognitive performance, higher weight, and stronger exploratory behavior tended to have longer lifespans. “These results suggest that being either smart or exhibiting good physical condition and exploratory behavior are likely to be different strategies that can lead to a longer lifespan,” said Claudia Fichtel, first author of the study and a scientist at the German Primate Center. “In future studies, we aim to investigate how cognitive abilities translate into behavioral strategies to find food or mating partner.”
Reinforcement learning establishes a minimal metacognitive process to monitor and control motor learning performance
by Taisei Sugiyama, Nicolas Schweighofer, Jun Izawa in Nature Communications
Monitoring and controlling one’s own learning process objectively is essential for improving one’s learning abilities. This ability, often referred to as “learning to learn” or “metacognition,” has been studied in educational psychology. Owing to the tight coupling between the higher meta-level and the lower object-level cognitive systems, a conventional reduction approach has difficulty understanding the neural basis of metacognition. To overcome this limitation, the researchers employed a novel research approach where they compared the metacognition of artificial intelligence (AI) to that of humans.
First, they demonstrated that the metacognitive system of AI, which aims to maximize rewards and minimize punishments, can effectively regulate learning speed and memory retention in response to the environment and task. Second, they demonstrated the metacognitive behavior of human motor learning, which demonstrates that providing monetary feedback as a function of memory can either promote or suppress motor learning and memory retention. This constitutes the first-ever empirical demonstration of the bi-directional regulation of implicit motor learning abilities by economic factors. Notably, while AI exhibited equal metacognitive abilities for reward and punishment, humans exhibited an asymmetric response to monetary gain and loss; humans adjust their memory retention in response to gain and their learning speed in response to loss. This asymmetric property may provide valuable insights into the neural mechanisms underlying human metacognition.
Researchers anticipate that these findings could be effectively applied to enhance the learning abilities of individuals engaging in new sports or motor-related activities, such as post-stroke rehabilitation training.
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