Learn about brain health and nootropics to boost brain function
Training of brain processes makes reading more efficient
The lexical categorization process and its implementation in the left-ventral occipito-temporal cortex. Credit: npj Science of Learning (2024). DOI: 10.1038/s41539-024-00237-7 A team of researchers from the University of Cologne and the University of Würzburg have found in training studies that the distinction between known and unknown words can be trained and leads to more efficient reading. Recognizing words is necessary to understand the meaning of a text. When we read, we move our eyes very efficiently and quickly from word to word.
This reading flow is interrupted when we encounter a word we do not know, a situation common when learning a new language. The words of the new language might have yet to be comprehended in their entirety, and language-specific peculiarities in spelling still need to be internalized. The team of psychologists led by junior professor Dr. Benjamin Gagl from the University of Cologne’s Faculty of Human Sciences has now found a method to optimize this process.
The current research results were published in npj Science of Learning under the title “Investigating lexical categorization in reading based on joint diagnostic and training approaches for language learners .” Starting in May, follow-up studies extending the training program will be carried out.
“Reading is essential for information processing,” said lead author Benjamin Gagl, who has been studying the cognitive and neural processes of word recognition for years. Two years ago, he and a team of researchers showed that in our understanding of the processes implemented in word recognition, psychological theories do not make sufficiently precise assumptions about the exact functions of one of the most frequently activated brain areas in the left temporal lobe.
To close this knowledge gap, Gagl and his colleagues developed a model that uses established behavioral findings from psychology to predict the activation of this reading area in the brain; this model serves as the basis for the training program described in the new study. Word filters as a building block for efficient reading
The model assumes that this brain region functions like a filter and separates already-known words from irrelevant or not-yet-known letter combinations; only known words are allowed to ‘pass’ to initiate consequential linguistic processing. However, when we encounter a new word, we cannot continue reading but would need to look up the word in a lexicon or on the Internet to understand its meaning.
The training procedures central to the current study were motivated by the assumptions of the “Lexical Categorization Model.” Behavioral studies showed that reading skills improved when participants were trained in this filtering process central to efficient reading. The training procedure included simple tasks in which readers should distinguish words from non-words (e.g., path vs. poth) by pressing a button.
After three training days, reading performance substantially improved in three separate studies. The team also used a machine learning-based diagnostic procedure that can increase the efficiency of training as it can detect participants who would likely not benefit from further training. This allows a decision to be made individually for each learner as to whether the lexical categorization training is worth the effort or whether alternative training should be carried out instead. New ways to compensate for reading problems
As part of a newly acquired project starting on 1 May, the researchers will further develop the computer models, motivating new training approaches for language learning or for the compensation of other reading disorders. In addition to the field of German as a foreign language, the training approaches can potentially be used in dyslexia treatment.
“Neuro-cognitive computer models can be used to implement basic scientific findings to be used in individual diagnostic training programs in educational and clinical settings. This enables us to help individual learners to optimize their reading skills and thus significantly improve their information processing skills,” said Gagl.
More information: Benjamin Gagl et al, Investigating lexical categorization in reading based on joint diagnostic and training approaches for language learners, npj Science of Learning (2024). DOI: 10.1038/s41539-024-00237-7
Provided by University of Cologne
Protecting brain cells with cannabinol: Research suggests CBN shows promise for treating neurological disorders
The outline of a person and their brain facing a cannabis leaf and symbolic CBN pill, demonstrating the potential for CBN to treat neurological disorders in the future. Credit: Salk Institute One in every 10 individuals above the age of 65 develops an age-related neurological disorder like Alzheimer’s or Parkinson’s, yet treatment options remain sparse for this population. Scientists have begun exploring whether cannabinoids—compounds derived from the cannabis plant, like well-known THC (tetrahydrocannabinol) and CBD (cannabidiol)—may offer a solution. A third, lesser-known cannabinoid called CBN (cannabinol) has recently piqued the interest of researchers, who have begun exploring the clinical potential of the milder, less psychoactive substance.
In a new study, scientists at the Salk Institute help explain how CBN protects the brain against aging and neurodegeneration, then use their findings to develop potential therapeutics. The researchers created four CBN-inspired compounds that were more neuroprotective than the standard CBN molecule—one of which was highly effective in treating traumatic brain injury in a Drosophila fruit fly model.
The findings, published in Redox Biology , suggest promise for CBN in treating neurological disorders like traumatic brain injury, Alzheimer’s disease, and Parkinson’s disease, and also highlight how further studies of CBN’s effects on the brain could inspire the development of new therapies for clinical use.
“Not only does CBN have neuroprotective properties, but its derivatives have the potential to become novel therapeutics for various neurological disorders,” says Research Professor Pamela Maher, senior author of the study. “We were able to pinpoint the active groups in CBN that are doing that neuroprotection, then improve them to create derivative compounds that have greater neuroprotective ability and drug-like efficacy.”
Many neurological disorders involve the death of brain cells called neurons, due to the dysfunction of their power-generating mitochondria. CBN achieves its neuroprotective effect by preventing this mitochondrial dysfunction —but how exactly CBN does this, and whether scientists can improve CBN’s neuroprotective abilities, has remained unclear.
The Salk team previously found that CBN was modulating multiple features of mitochondrial function to protect neurons against a form of cell death called oxytosis/ferroptosis. After uncovering this mechanism of CBN’s neuroprotective activity, they began applying both academic and industrial drug discovery methods to further characterize and attempt to improve that activity.
First, they broke CBN into small fragments and observed which of those fragments were the most effective neuroprotectors by chemically analyzing the fragment’s properties. Second, they designed and constructed four novel CBN analogs—chemical look-alikes—in which those fragments were amplified, then moved them on to drug screening.
“We were looking for CBN analogs that could get into the brain more efficiently, act more quickly, and produce a stronger neuroprotective effect than CBN itself,” says Zhibin Liang, first author and postdoctoral researcher in Maher’s lab. “The four CBN analogs we landed on had improved medicinal chemical properties, which was exciting and really important to our goal of using them as therapeutics.”
To test the chemical medicinal properties of the four CBN analogs, the team applied them to mouse and human nerve cell cultures. When they initiated oxytosis/ferroptosis in three different ways, they found that each of the four analogs 1) were able to protect the cells from dying, and 2) had similar neuroprotective abilities compared to regular CBN.
The successful analogs were then put to the test in a Drosophila fruit fly model of traumatic brain injury. One of the analogs, CP1, was especially effective in treating traumatic brain injury —producing the highest survival rate after condition onset.
“Our findings help demonstrate the therapeutic potential of CBN, as well as the scientific opportunity we have to replicate and refine its drug-like properties,” says Maher. “Could we one day give this CBN analog to football players the day before a big game, or to car accident survivors as they arrive in the hospital? We’re excited to see how effective these compounds might be in protecting the brain from further damage.”
In the future, the researchers will continue to screen and characterize these CBN analogs and refine their chemical designs. They will also begin looking more closely at age-related neurodegeneration and changes in brain cells, particularly in mitochondria, asking how we can better suit these drug-like compounds to promote cellular health and prevent neuronal dysfunction with age.
Other authors include David Soriano-Castell and Wolfgang Fischer of Salk; and Alec Candib and Kim Finley of the Shiley Bioscience Center at San Diego State University.
Provided by Salk Institute
Salk scientists explain how CBN protects the brain against aging and neurodegeneration
One in every 10 individuals above the age of 65 develops an age-related neurological disorder like Alzheimer’s or Parkinson’s, yet treatment options remain sparse for this population. Scientists have begun exploring whether cannabinoids-;compounds derived from the cannabis plant, like well-known THC (tetrahydrocannabinol) and CBD (cannabidiol)-;may offer a solution. A third, lesser-known cannabinoid called CBN (cannabinol) has recently piqued the interest of researchers, who have begun exploring the clinical potential of the milder, less psychoactive substance.
In a new study, scientists at the Salk Institute help explain how CBN protects the brain against aging and neurodegeneration, then use their findings to develop potential therapeutics. The researchers created four CBN-inspired compounds that were more neuroprotective than the standard CBN molecule-;one of which was highly effective in treating traumatic brain injury in a Drosophila fruit fly model.
The findings, published in Redox Biology on March 29, 2024, suggest promise for CBN in treating neurological disorders like traumatic brain injury, Alzheimer’s disease, and Parkinson’s disease, and also highlight how further studies of CBN’s effects on the brain could inspire the development of new therapies for clinical use. Not only does CBN have neuroprotective properties, but its derivatives have the potential to become novel therapeutics for various neurological disorders. We were able to pinpoint the active groups in CBN that are doing that neuroprotection, then improve them to create derivative compounds that have greater neuroprotective ability and drug-like efficacy .” Pamela Maher, Research Professor, senior author of the study Many neurological disorders involve the death of brain cells called neurons, due to the dysfunction of their power-generating mitochondria. CBN achieves its neuroprotective effect by preventing this mitochondrial dysfunction-;but how exactly CBN does this, and whether scientists can improve CBN’s neuroprotective abilities, has remained unclear.
The Salk team previously found that CBN was modulating multiple features of mitochondrial function to protect neurons against a form of cell death called oxytosis/ferroptosis. After uncovering this mechanism of CBN’s neuroprotective activity, they began applying both academic and industrial drug discovery methods to further characterize and attempt to improve that activity.
First, they broke CBN into small fragments and observed which of those fragments were the most effective neuroprotectors by chemically analyzing the fragment’s properties. Second, they designed and constructed four novel CBN analogs-;chemical look-alikes-;in which those fragments were amplified, then moved them on to drug screening.
“We were looking for CBN analogs that could get into the brain more efficiently, act more quickly, and produce a stronger neuroprotective effect than CBN itself,” says Zhibin Liang, first author and postdoctoral researcher in Maher’s lab. “The four CBN analogs we landed on had improved medicinal chemical properties, which was exciting and really important to our goal of using them as therapeutics.”
To test the chemical medicinal properties of the four CBN analogs, the team applied them to mouse and human nerve cell cultures. When they initiated oxytosis/ferroptosis in three different ways, they found that each of the four analogs 1) were able to protect the cells from dying, and 2) had similar neuroprotective abilities compared to regular CBN.
The successful analogs were then put to the test in a Drosophila fruit fly model of traumatic brain injury. One of the analogs, CP1, was especially effective in treating traumatic brain injury-;producing the highest survival rate after condition onset.
“Our findings help demonstrate the therapeutic potential of CBN, as well as the scientific opportunity we have to replicate and refine its drug-like properties,” says Maher. “Could we one day give this CBN analog to football players the day before a big game, or to car accident survivors as they arrive in the hospital? We’re excited to see how effective these compounds might be in protecting the brain from further damage.”
In the future, the researchers will continue to screen and characterize these CBN analogs and refine their chemical designs. They will also begin looking more closely at age-related neurodegeneration and changes in brain cells, particularly in mitochondria, asking how we can better suit these drug-like compounds to promote cellular health and prevent neuronal dysfunction with age.
Other authors include David Soriano-Castell and Wolfgang Fischer of Salk; and Alec Candib and Kim Finley of the Shiley Bioscience Center at San Diego State University.
The work was supported by the Paul F. Glenn Center for Biology of Aging Research at the Salk Institute, the Bundy Foundation, the Shiley Foundation, the National Institutes of Health (R01AG067331, R21AG064287, R01AG069206, RF1AG061296, R21AG067334, NCI CCSG P30CA01495, NlA P30AG068635, S10OD021815), and the Helmsley Center for Genomic Medicine.
Source:
Salk Institute
Journal reference:
Liang, Z., et al. (2024). Fragment-based drug discovery and biological evaluation of novel cannabinol-based inhibitors of oxytosis/ferroptosis for neurological disorders. Redox Biology . doi.org/10.1016/j.redox.2024.103138 .
Protecting brain cells with cannabinol
One in every 10 individuals above the age of 65 develops an age-related neurological disorder like Alzheimer’s or Parkinson’s, yet treatment options remain sparse for this population. Scientists have begun exploring whether cannabinoids — compounds derived from the cannabis plant, like well-known THC (tetrahydrocannabinol) and CBD (cannabidiol) — may offer a solution. A third, lesser-known cannabinoid called CBN (cannabinol) has recently piqued the interest of researchers, who have begun exploring the clinical potential of the milder, less psychoactive substance.
In a new study, scientists at the Salk Institute help explain how CBN protects the brain against aging and neurodegeneration, then use their findings to develop potential therapeutics. The researchers created four CBN-inspired compounds that were more neuroprotective than the standard CBN molecule — one of which was highly effective in treating traumatic brain injury in a Drosophila fruit fly model.
The findings, published in Redox Biology on March 29, 2024, suggest promise for CBN in treating neurological disorders like traumatic brain injury, Alzheimer’s disease, and Parkinson’s disease, and also highlight how further studies of CBN’s effects on the brain could inspire the development of new therapies for clinical use.
“Not only does CBN have neuroprotective properties, but its derivatives have the potential to become novel therapeutics for various neurological disorders,” says Research Professor Pamela Maher, senior author of the study. “We were able to pinpoint the active groups in CBN that are doing that neuroprotection, then improve them to create derivative compounds that have greater neuroprotective ability and drug-like efficacy.”
Many neurological disorders involve the death of brain cells called neurons, due to the dysfunction of their power-generating mitochondria. CBN achieves its neuroprotective effect by preventing this mitochondrial dysfunction — but how exactly CBN does this, and whether scientists can improve CBN’s neuroprotective abilities, has remained unclear.
The Salk team previously found that CBN was modulating multiple features of mitochondrial function to protect neurons against a form of cell death called oxytosis/ferroptosis. After uncovering this mechanism of CBN’s neuroprotective activity, they began applying both academic and industrial drug discovery methods to further characterize and attempt to improve that activity.
First, they broke CBN into small fragments and observed which of those fragments were the most effective neuroprotectors by chemically analyzing the fragment’s properties. Second, they designed and constructed four novel CBN analogs — chemical look-alikes — in which those fragments were amplified, then moved them on to drug screening.
“We were looking for CBN analogs that could get into the brain more efficiently, act more quickly, and produce a stronger neuroprotective effect than CBN itself,” says Zhibin Liang, first author and postdoctoral researcher in Maher’s lab. “The four CBN analogs we landed on had improved medicinal chemical properties, which was exciting and really important to our goal of using them as therapeutics.”
To test the chemical medicinal properties of the four CBN analogs, the team applied them to mouse and human nerve cell cultures. When they initiated oxytosis/ferroptosis in three different ways, they found that each of the four analogs 1) were able to protect the cells from dying, and 2) had similar neuroprotective abilities compared to regular CBN.
The successful analogs were then put to the test in a Drosophila fruit fly model of traumatic brain injury. One of the analogs, CP1, was especially effective in treating traumatic brain injury — producing the highest survival rate after condition onset.
“Our findings help demonstrate the therapeutic potential of CBN, as well as the scientific opportunity we have to replicate and refine its drug-like properties,” says Maher. “Could we one day give this CBN analog to football players the day before a big game, or to car accident survivors as they arrive in the hospital? We’re excited to see how effective these compounds might be in protecting the brain from further damage.”
In the future, the researchers will continue to screen and characterize these CBN analogs and refine their chemical designs. They will also begin looking more closely at age-related neurodegeneration and changes in brain cells, particularly in mitochondria, asking how we can better suit these drug-like compounds to promote cellular health and prevent neuronal dysfunction with age.
Other authors include David Soriano-Castell and Wolfgang Fischer of Salk; and Alec Candib and Kim Finley of the Shiley Bioscience Center at San Diego State University.
The work was supported by the Paul F. Glenn Center for Biology of Aging Research at the Salk Institute, the Bundy Foundation, the Shiley Foundation, the National Institutes of Health (R01AG067331, R21AG064287, R01AG069206, RF1AG061296, R21AG067334, NCI CCSG P30CA01495, NlA P30AG068635, S10OD021815), and the Helmsley Center for Genomic Medicine.
Human brains and fruit fly brains are built similarly—researchers are studying the differences
This figure shows connections between different mushroom body neurons. Credit: Scaplen et al. 2021/eLife , CC BY The human brain contains approximately 87 billion neurons . On average, each of these cells make thousands of different connections to facilitate communication across the brain. Neural communication is thought to underlie all brain functions—from experiencing and interpreting the world around you to remembering those experiences and controlling how your body responds.
But in this vast network of neural communication, precisely who is talking to whom, and what is the consequence of those individual conversations?
Understanding the details surrounding neural communication and how it’s shaped by experience is one of the many focuses of neuroscience. However, this is complicated by the sheer number of microscopic connections there are to study in the human brain , many of which are often in flux, and that available tools are unable to provide adequate resolution.
As a consequence, many scientists like me have turned to simpler organisms, such as the fruit fly.
Fruit flies, though pesky in the kitchen, are invaluable in the laboratory. Their brains are built in remarkably similar ways to those of humans. Importantly, scientists have developed tools that make fly brains significantly easier to study with a resolution that hasn’t been achieved in other organisms.
My colleague Gilad Barnea, a neuroscientist at Brown University, and his team spent over 20 years developing a tool to visualize all of the microscopic connections between neurons within the brain. The video starts close to the face of the fly and moves back, using genetics to express different proteins within neurons to visualize them. Green indicates the neuron of interest, red indicates the neuron it talks to and blue indicates all other brain cells. Credit: Kristin Scaplen , CC BY-SA Neurons communicate with each other by sending and receiving molecules called neurotransmitters between receptor proteins on their surface. Barnea’s tool, trans-Tango , translates the activation of specific receptor proteins into gene expression that ultimately allow for visualization.
My team and I used trans-Tango to visualize all the neural connections of a learning and memory center, called the mushroom body , in the fruit fly brain.
Here, a cluster of approximately four neurons, labeled green, receive messages from the mushroom body, which is the L-shaped structure labeled blue in the center of the fly brain. You can step through the brain and see all the other neurons they likely communicate with, labeled red.
The cell bodies of the neurons reside on the edges of the brain, and the locations where they receive messages from the mushroom body appear as green tangles invading a small oval compartment. Where these weblike green extensions mingle with red are thought to be where neurons communicate their processed message to other downstream neurons.
Stepping further into the brain, you can see the downstream neurons navigating to a single layer of a fan-shaped structure within the brain. This fan-shaped body is thought to modulate many functions, including arousal , memory storage , locomotion and transforming sensory experiences into actions .
Not only did our images reveal previously unknown connections across the brain, but it also provides an opportunity to explore the consequences of those individual neural conversations. Fly brain connections were remarkably consistent but also varied slightly from one fly to another. These slight variations in connectivity are likely influenced by the fly’s individual experiences , just like they are in people.
The beauty of trans-Tango lies in its flexibility. In addition to visualizing connections, scientists can use genes to manipulate neural activity and better understand how neural communication affects behavior. Because fly brains are similarly built to those of humans, researchers can use them to study how brain connections function and how they might be disrupted in disease. Ultimately, this will improve our understanding of our own brains and the human condition.
Provided by The Conversation
This article is republished from The Conversation under a Creative Commons license. Read the original article .
Boosting the brain’s control of prosthetic devices by tapping the cerebellum
Direct and indirect modulation of M1 and cerebellar activity with neuroprosthetic learning. Credit: Science Advances (2024). DOI: 10.1126/sciadv.adm8246 Neuroprosthetics, a technology that allows the brain to control external devices such as robotic limbs, is beginning to emerge as a viable option for patients disabled by amputation or neurological conditions such as stroke. Cedars-Sinai investigators, in a study published in the journal Science Advances , are believed to be the first to show that tapping the power of the cerebellum, a region in the back of the brain, could improve patients’ ability to control these devices.
“Neuroprosthetics have largely tapped the brain’s outermost cerebral cortex. The cerebellum has a well-known role in movement but has been ignored in neuroprosthetic research,” said Tanuj Gulati, Ph.D., assistant professor of Biomedical Sciences and Neurology and researcher in the Center for Neural Science and Medicine at Cedars-Sinai, and senior author of the study.
“We are the first to record what is happening in the cerebellum as the brain learns to manipulate these devices, and we found that its involvement is essential for device use .”
Patients who use neuroprosthetic devices have electrodes permanently implanted in the portion of the brain—usually the cerebral cortex—that controls movement for the function the device is replacing. This technique can be used to help patients control a robotic limb, a motorized wheelchair or a computer keyboard, among other devices.
To learn how the cerebellum helps in learning neuroprosthetic control, Gulati and his team trained laboratory rats to use only their motor cortex activity to move a neuroprosthetic tube that delivered them water. The rats had electrodes implanted in the motor cortex and the cerebellum, and investigators listened in on the activity of neurons in both brain regions during the experiments.
“We found that activity of the neurons in the cerebellum was coordinated with the motor cortex, and that activity in the cerebellum was critical for neuroprosthetic task performance,” said Aamir Abbasi, Ph.D., a postdoctoral scientist in the Gulati Lab and the first author of the study. Coordinated neuroprosthetic task-related oscillations emerge in M1 and cerebellar LFPs. Credit: Science Advances (2024). DOI: 10.1126/sciadv.adm8246 Investigators next used an advanced technology called optogenetics to selectively silence different neuron populations in the laboratory rats’ brains during experiments. Optogenetics delivers light-sensitive proteins into brain cells, allowing light exposure to control these cells’ activity.
When they silenced neurons in the outer layer of the cerebellum, where the cerebellum receives input from other brain regions, they found that the laboratory rats had a difficult time learning to control movement of the pipe. When they silenced neurons deep in the cerebellum, which are responsible for outward communication from the cerebellum to the motor cortex, the rats had difficulty maintaining accurate control of the pipe.
“These results could help make neuroprosthetics an option for patients with damage to the motor cortex due to brain injury , stroke or diseases such as Parkinson’s or multiple sclerosis,” said Nancy L. Sicotte, MD, chair of the Department of Neurology and the Women’s Guild Distinguished Chair in Neurology at Cedars-Sinai.
“It’s possible that, eventually, implants in the cerebellar region could be used to help these patients manipulate external devices.”
It’s an exciting era for neuroprosthetics, said David Underhill, Ph.D., chair of the Department of Biomedical Sciences at Cedars-Sinai.
“There is a lot of buzz about neuroprosthetic technology, but there are still many unsolved problems,” Underhill said. “This study suggests that some of those could be resolved by involving the cerebellum as well as the motor cortex to help patients gain use of neuroprosthetic devices more quickly and improve their ability to control them accurately.”
Provided by Cedars-Sinai Medical Center
Breakthrough brain stimulator could revolutionize treatment for neurological disorders
Rice University engineers have developed the smallest implantable brain stimulator demonstrated in a human patient. Thanks to pioneering magnetoelectric power transfer technology, the pea-sized device developed in the Rice lab of Jacob Robinson in collaboration with Motif Neurotech and clinicians Dr. Sameer Sheth and Dr. Sunil Sheth can be powered wirelessly via an external transmitter and used to stimulate the brain through the dura ⎯ the protective membrane attached to the bottom of the skull.
The device, known as the Digitally programmable Over-brain Therapeutic (DOT), could revolutionize treatment for drug-resistant depression and other psychiatric or neurological disorders by providing a therapeutic alternative that offers greater patient autonomy and accessibility than current neurostimulation-based therapies and is less invasive than other brain-computer interfaces (BCIs). In this paper we show that our device, the size of a pea, can activate the motor cortex, which results in the patient moving their hand. In the future, we can place the implant above other parts of the brain, like the prefrontal cortex, where we expect to improve executive functioning in people with depression or other disorders.” Jacob Robinson, professor of electrical and computer engineering and of bioengineering, Rice University Existing implantable technologies for brain stimulation are powered by relatively large batteries that need to be placed under the skin elsewhere in the body and connected to the stimulating device via long wires. Such design limitations require more surgery and subject the individual to a greater burden of hardware implantation, risks of wire breakage or failure and the need for future battery replacement surgeries.
“We eliminated the need for a battery by wirelessly powering the device using an external transmitter,” explained Joshua Woods, an electrical engineering graduate student in the Robinson lab and lead author on the study published in Science Advances . Amanda Singer, a former graduate student in Rice’s applied physics program who is now at Motif Neurotech, is also a lead author.
The technology relies on a material that converts magnetic fields into electrical pulses. This conversion process is very efficient at small scales and has good misalignment tolerance, meaning it does not require complex or minute maneuvering to activate and control. The device has a width of 9 millimeters and can deliver 14.5 volts of stimulation.
“Our implant gets all of its energy through this magnetoelectric effect,” said Robinson, who is founder and CEO of Motif, a startup working to bring the device to market. “The physics of that power transfer makes this much more efficient than any other wireless power transfer technologies under these conditions.”
Motif is one of several neurotech companies that are probing the potential of BCIs to revolutionize treatments for neurological disorders.
“Neurostimulation is key to enabling therapies in the mental health space where drug side effects and a lack of efficacy leave many people without adequate treatment options,” Robinson said.
The researchers tested the device temporarily in a human patient, using it to stimulate the motor cortex ⎯ the part of the brain responsible for movement ⎯ and generating a hand movement response. They next showed the device interfaces with the brain stably for a 30-day duration in pigs.
“This has not been done before because the quality and strength of the signal needed to stimulate the brain through the dura were previously impossible with wireless power transfer for implants this small,” Woods said.
Robinson envisions the technology being used from the comfort of one’s home. A physician would prescribe the treatment and provide guidelines for using the device, but patients would retain complete control over how the treatment is administered.
“Back home, the patient would put on their hat or wearable to power and communicate with the implant, push ‘go’ on their iPhone or their smartwatch and then the electrical stimulation from that implant would activate a neuronal network inside the brain,” Robinson said.
Implantation would require a minimally invasive 30-minute procedure that would place the device in the bone over the brain. Both the implant and the incision would be virtually invisible, and the patient would go home the same day.
“When you think about a pacemaker, it’s a very routine part of cardiac care,” said Sheth, professor and vice-chair of research, McNair Scholar and Cullen Foundation Endowed Chair of Neurosurgery at the Baylor College of Medicine. “In neurological and psychiatric disorders, the equivalent is deep brain stimulation (DBS), which sounds scary and invasive. DBS is actually quite a safe procedure, but it’s still brain surgery, and its perceived risk will place a very low ceiling on the number of people who are willing to accept it and may benefit from it. Here’s where technologies like this come in. A 30-minute minor procedure that is little more than skin surgery, done in an outpatient surgery center, is much more likely to be tolerated than DBS. So if we can show that it is about as effective as more invasive alternatives, this therapy will likely make a much larger impact on mental health.”
For some conditions, epilepsy for example, the device may need to be on permanently or most of the time, but for disorders such as depression and OCD, a regimen of just a few minutes of stimulation per day could suffice to bring about the desired changes in the functioning of the targeted neuronal network.
In terms of next steps, Robinson said that on the research side he is “really interested in the idea of creating networks of implants and creating implants that can stimulate and record, so that they can provide adaptive personalized therapies based on your own brain signatures.” From the therapeutic development standpoint, Motif Neurotech is in the process of seeking FDA approval for a long-term clinical trial in humans. Patients and caregivers can sign up on the Motif Neurotech website to learn when and where these trials will begin.
The work was supported in part by The Robert and Janice McNair Foundation, the McNair Medical Institute, DARPA and the National Science Foundation.
Source:
Rice University
Journal reference:
Woods, J. E., et al. (2024) Miniature battery-free epidural cortical stimulators. Science Advances. doi.org/10.1126/sciadv.adn0858 .
Exercise changes the brain in a way that helps heart health, especially for people with depression
WATCH: This type of exercise might be better for your brain than biking or jogging Sign up for CNN’s Fitness, But Better newsletter series. Our seven-part guide will help you ease into a healthy routine, backed by experts .
CNN —
It’s common knowledge that exercise is good for your mental health and your heart health — and now a new study suggests that all three are working together.
In addition to the physical benefits of exercise, it’s also associated with a reduction in stress signals in the brain, which leads to a decreased risk of cardiovascular disease, according to the study.
Researchers analyzed data of more than 50,000 adults around age 60 from the Mass General Brigham Biobank, according to the study published Monday in the Journal of the American College of Cardiology. Related article Women might lower their risk for cardiovascular disease by twice the amount as men with exercise
The study looked at a survey that participants were given about their physical activity, imaging of their brains to track activity related to stress, and digital records of cardiovascular events.
“Individuals who exercise more had a graded reduction in stress related signals in the brain,” said lead study author Dr. Ahmed Tawakol, a cardiologist at Mass General Hospital and associate professor of medicine at Harvard Medical School in Boston.
“We found nice associations that exercise appeared to, in part, reduce heart disease risks by decreasing stress-related signals,” he added.
Everyone should pay attention whenever studies come out that show this kind of improvement resulting from a change in lifestyle, said Dr. Andrew Freeman, director of cardiovascular prevention and wellness at National Jewish Health in Denver. Freeman was not involved in this study.
“These are incredibly cost effective, the magnitude of improvements are amazing — often better than many medications — and we should be putting these tools in our arsenal for ready use,” he said. Twofold for people with depression
Tawakol and his team also wanted to know whether people with more stress-related signals in the brain would get a greater benefit from exercise, he said.
“Surprisingly, we additionally found a greater than twofold increase in benefits of exercise among individuals who are depressed versus individuals who don’t have depression or don’t have a history of depression,” Tawakol said.
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The relationship between amount of exercise and decrease in the level of cardiovascular risk also varied depending on whether a person had a history of depression, he added.
For people without any history of depression, the benefit of exercise on cardiovascular disease reduction plateaued after about 300 minutes of moderate physical activity a week. But for people with depression, the benefits continued with more time spent, Tawakol said. Find exercise you will enjoy and do regularly, said Dr. Andrew Freeman, director of cardiovascular prevention and wellness at National Jewish Health in Denver. He wasn’t involved in the study. Oleg Breslavtsev/Moment RF/Getty Images
These benefits are in addition to the psychological benefits researchers already know exercise provides, he added.
“We know depression is an important risk factor for heart disease and it is also one of the most common stress-related conditions,” said study coauthor Dr. Karmel Choi, clinical psychologist and assistant professor at Harvard Medical School and Massachusetts General Hospital.
“Even though some people may be more susceptible to stress and its health consequences, here we see they may also stand to benefit more from exercise and its stress-modulating effects. Which is encouraging,” she added in an email. How it works
Exercise reduced stress signals and increased prefrontal cortical signals, Tawakol said.
“Both are attractive changes in the brain,” he said.
The prefrontal cortex is the part of the brain responsible for executive function, which are the cognitive processes that control behavior, Tawakol said.
And stress signals in the brain ar e associated with things like inflammation,higher sympathetic nervous system activity, higher blood pressure, and diseases that thicken or harden the arteries, he added.
In part, exercise appeared to reduce heart disease risks by reducing the stress signals, Tawakol said.
These findings are just associations, however. Because the researchers observed participants rather than conducting a randomized trial with a control group, they cannot say for sure that the exercise caused the reductions or what the mechanisms are that underlie it, he said. What exercise will make a difference?
You don’t have to be a pro athlete to have a good exercise routine, and it can help to work your way up, Freeman said. Related article Are you making one of these common exercising errors? Experts weigh in “It turns out human beings were designed to move and move a lot, and when we do — particularly when we are outside and amongst trees — there’s been data to suggest these all have very significant stress-relieving effects.”Freeman recommends checking with your doctor first and trying to get to 30 minutes a day of breathless physical activity — and it doesn’t matter what that activity is.“If you don’t enjoy walking or biking or swimming or whatever it is, don’t do it. But figure out a way to get a physical activity in that you truly enjoy,” he said.Just make sure that it feels difficult for you whatever your fitness level may be, Freeman added. If you can talk in full sentences while exercising, it might be time to make it harder, he said.
Researchers Discover New Origin of Deep Brain Waves
UC Irvine researchers have discovered that crucial brain waves for deep sleep, previously believed to be generated only by a specific brain circuit, also originate from the hippocampus, offering new insights into memory processing during sleep. Understanding hippocampal activity could improve sleep and cognition therapies.
Researchers from the University of California, Irvine’s biomedical engineering department have discovered a new origin for two essential brain waves—slow waves and sleep spindles—that are critical for deep sleep. While it was traditionally thought that these brain waves originated solely from a circuit connecting the thalamus and cortex, the team’s findings, published in Scientific Reports , suggest that the axons in memory centers of the hippocampus play a role.
For decades, slow waves and sleep spindles have been identified as essential elements of deep sleep, measured through electroencephalography recordings on the scalp. However, the UC Irvine-led team revealed a novel source of these brain waves within the hippocampus and were able to measure them in single axons.
The study demonstrates that slow waves and sleep spindles can originate from axons within the hippocampus’ cornu ammonis 3 region. These oscillations in voltage occur independently of neuronal spiking activity, challenging existing theories about the generation of these brain waves. Research Methodology and Findings
“Our research sheds light on a previously unrecognized aspect of deep sleep brain activity,” said lead author Mengke Wang, former UC Irvine undergraduate student in biomedical engineering who is now a graduate student at Johns Hopkins University (Wang conducted the study while at UC Irvine). “We’ve discovered that the hippocampus, typically associated with memory formation, plays a crucial role in generating slow waves and sleep spindles, offering new insights into how these brain waves support memory processing during sleep.”
The team utilized innovative techniques – including in vitro reconstructions of hippocampal subregions and microfluidic tunnels for single axon communication – to observe spontaneous spindle waves in isolated hippocampal neurons. These findings suggest that spindle oscillations originate from active ion channels within axons, rather than through volume conduction as previously thought. Implications and Future Research
“The discovery of spindle oscillations in single hippocampal axons opens new avenues for understanding the mechanisms underlying memory consolidation during sleep,” said co-author Gregory Brewer, adjunct professor of biomedical engineering. “These findings have significant implications for sleep research, potentially paving the way for new approaches to treating sleep-related disorders.”
Brewer’s other research affiliations include the Institute for Memory Impairment and Neurological Disorders and the Center for Neurobiology of Learning and Memory.
By uncovering the hippocampus’s role in generating slow waves and sleep spindles, this research expands our understanding of the brain’s activity during deep sleep and its impact on memory processing. The findings offer a promising foundation for future studies exploring the therapeutic potential of targeting hippocampal activity to improve sleep quality and cognitive function.
Reference: “Spindle oscillations in communicating axons within a reconstituted hippocampal formation are strongest in CA3 without thalamus” by Mengke Wang, Samuel B. Lassers, Yash S. Vakilna, Bryce A. Mander, William C. Tang and Gregory J. Brewer, 10 April 2024, Scientific Reports .
DOI: 10.1038/s41598-024-58002-0
Joining Brewer and Wang in this study, which received financial support from the UCI Foundation, were William Tang, professor emeritus of biomedical engineering; Bryce Mander, associate professor of psychiatry & human behavior; and Samuel Lassers, graduate student researcher in biomedical engineering.
Study: Most gender-confused children OUTGROW gender dysphoria during adulthood
A 15-year-period study published in the journal Archives of Sexual Behavior reveals that “most” gender-confused children outgrow such feelings by the time they reach adulthood.
The study, conducted by Dutch researchers from the University of Groningen , tracked 2,770 children from the age of 11 until their mid-twenties. Every three years, from March 2001 to 2015, participants would respond to the same statement at six different points: “I wish to be of the opposite sex.” Participants will only choose from three options: 0-Not True, 1-Somewhat or Sometimes True, and 2-Very True or Often True. Additionally, participants rate their feelings regarding physical appearance and self-esteem to evaluate their self-worth.
Initially, the research found that about 11 percent of children experienced varying degrees of “gender non-contentedness,” a dissatisfaction with their biological sex alignment, during puberty. However, as these children reached the age of 25, the figure significantly decreased to four percent.
Thus, the study concludes that fluctuations in gender non-contentedness were associated with lower self-worth, more behavioral problems and increased emotional struggles, particularly among females. However, findings also suggest that doubts about one’s gender identity during adolescence are relatively common but tend to diminish with age .
“The results of the current study might help adolescents to realize that it is normal to have some doubts about one’s identity and one’s gender identity during this age period and that this is also relatively common,” the researchers concluded. Experts warn colleagues about rushing children and adolescents into gender transition
This study adds to the long list of studies debunking the claims of left-wing advocates that gender “affirming” treatments like hormones and surgical interventions effectively address the mental health issues of children with gender dysphoria. (Related: American College of Pediatrics DEBUNKS claim that “affirmation” helps the mental health of children with gender dysphoria .)
Patrick Brown, a fellow at the conservative Ethics and Public Policy Center, warned the public against aggressive steps toward facilitating gender transition in childhood and adolescence.
“This study provides even more reason to be skeptical towards aggressive steps to facilitate gender transition in childhood and adolescence. The fact that rates of satisfaction are lower even just a few years later suggests that for the vast majority of people, prudence and caution, rather than a rush towards permanent surgeries or hormone therapies, will be the best approach for teenagers struggling to make sense of the world and their place in it,” Brown said. “As such, policies that prohibit gender transition for minors make a great deal of sense.”
Meanwhile, Jay Richards, the director of the Richard and Helen DeVos Center for Life, Religion and Family, cited historical data suggesting a significant proportion of gender-dysphoric children desist from such feelings as they undergo natural puberty. So, he warned medical experts against medicalizing temporary psychological symptoms.
“We’ve known for over a decade that most kids who experience distress with their sexed bodies resolve those feelings after they pass through natural puberty. Indeed, we can infer from the DSM 5 [2013] and other sources that as many as 88 percent of gender-dysphoric girls and as many as 98 percent of gender-dysphoric boys in previous generations desisted if allowed to go through natural puberty. These two facts make it clear why “gender-affirming care” for minors is such an outrage.
“It leads, in the end, to sterilization and in many cases to a complete loss of natural sexual function. There is no good evidence that this helps minors long term. Moreover, it medicalizes what could very well be temporary psychological symptoms,” he said.
Watch this video featuring Jennifer Bilek as she talks about who is behind the trans agenda .
This video is from the Hamilton-Moore Effect channel on Brighteon.com . More related stories:
Gender dysphoria is a “social contagion” spreading through peer pressure and propaganda, warns expert .
Better late than never: UK to stop prescribing puberty blockers for children who experience gender dysphoria .
New York pediatrician says gender transition is a “normal thing” that “starts at birth or even before.”
Gender transition indoctrination is extreme child abuse, warns psychiatrist .
GENDER-AFFIRMING BRAINWASH: The term “gender-affirming care” is NOT care at all, but mutilation, and “affirming” is NOT medicine, just delusion and child abuse .
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Neuroscience Study Taps Into Brain Network Patterns to Understand Deep Focus, Attention
A team of Georgia Tech researchers is the first to study the relationship between fluctuations in attention and the brain network patterns within low-frequency 20-second cycles. Photo credit: Paul Skorupskas, unsplash.com From completing puzzles and playing music, to reading and exercising, growing up Dolly Seeburger loved activities that demanded her full attention. “It was in those times that I felt most content, like I was in the zone,” she remembers. “Hours would pass, but it would feel like minutes.”
While this deep focus state is essential to highly effective work, it’s still not fully understood. Now, a new study led by Seeburger, a graduate student in the School of Psychology , alongside her advisor, Eric Schumacher , a professor in the School of Psychology is unearthing the mechanisms behind it.
The interdisciplinary Georgia Tech team also includes Nan Xu, Sam Larson and Shella Keilholz ( Coulter Department of Biomedical Engineering ), alongside Marcus Ma ( College of Computing ), and Christine Godwin ( School of Psychology ).
The researchers’ study, “ Time-varying functional connectivity predicts fluctuations in sustained attention in a serial tapping task ,” was published in Cognitive, Affective, and Behavioral Neuroscience earlier this year, and it investigates brain activity via fMRI during periods of deep focus and less-focused work.
The work is the first to investigate low-frequency fluctuations between different networks in the brain during focus, and could act as a springboard to study more complex behaviors and focus states.
“Your brain is dynamic! Nothing is just on or off,” Seeburger explains. “This is the phenomenon we wanted to study. How does one get into the zone? Why is it that some people can sustain their attention better than others? Is this something that can be trained? If so, can we help people get better at it?” The dynamic brain
The team’s work is also the first to study the relationship between fluctuations in attention and the brain network patterns within these low-frequency 20-second cycles. “For quite a while, the studies on neural oscillations focused on faster temporal frequencies, and the appreciation of these very low-frequency oscillations is relatively new,” Seeburger says. “But, these low-frequency fluctuations may play a key role in regulating higher cognition such as sustained attention.”
“One of the things we’ve discovered in previous research is that there’s a natural fluctuation in activity in certain brain networks. When a subject is not doing a specific task while in the MRI scanner, we see that fluctuation happen roughly every 20 seconds,” adds co-author Schumacher, explaining that the team was interested in the pattern because it is quasi-periodic, meaning that it doesn’t repeat exactly every 20 seconds, and it varies between different trials and subjects.
By studying these quasi-periodic cycles, the team hoped to measure the relationship between the brain fluctuation in these networks and the behavioral fluctuation associated with changes in attention. Your attention needed
To measure attention, participants tapped along to a metronome while in an fMRI scanner. The team could measure how “in the zone” participants were by measuring how much variability was in each participant’s taps — more variability suggested the participant was less focused, while precise tapping suggested the participant was “in the zone.”
The researchers found that when a subject’s focus level changed, different regions of the brain synchronized and desychronized, in particular the fronto-parietal control network (FPCN) and default mode network (DMN), The FPCN is engaged when a person is trying to stay on task, whereas the DMN is correlated with internally-oriented thoughts (which a participant might be having when less focused). “When one is out-of-the-zone, these two networks synchronize, and are in phase in the low frequency,” Seeburger explains. “When one is in the zone, these networks desynchronize.”
The results suggest that the 20-second patterns could help predict if a person is sustaining their attention or not, and could provide key insight for researchers developing tools and techniques that help us deeply focus. The big picture
While the direct relationship between behavior and brain activity is still unknown, these 20-second patterns in brain fluctuation are seen universally, and across species. “If you put someone in a scanner and their mind is wandering, you find these fluctuations. You can find these quasi-period patterns in rodents. You can find it in primates,” Schumacher says. “There’s something fundamental about this brain network activity.”
“I think it answers a really fundamental question about the relationship between behavior and brain activity,” he adds. “Understanding how these brain networks work together and impact behavior could lead to new therapies to help people organize their brain networks in the most efficient way.”
And while this simple task might not investigate complex behaviors, the study could act as a springboard to move into more complicated behaviors and focus states. “Next, I would like to study sustained attention in a more naturalistic way,” Seeburger says. “I hope that we can further the understanding of attention and help people get a better handle on their ability to control, sustain, and increase it.”
DOI: https://doi.org/10.3758/s13415-024-01156-1
Neuroscience Breakthrough Unveils How We Learn and Remember
New findings in memory research reveal the role of dendritic translation in learning, identifying thousands of micropeptides and key regulatory proteins, offering insights into intellectual disabilities and broader neurological functions. Credit: SciTechDaily.com Activity taking place within the dendrites that branch off of neuron cell bodies is key to memory formation.
Less than twenty minutes after finishing this article, your brain will begin to store the information that you’ve just read in a coordinated burst of neuronal activity. Underpinning this process is a phenomenon known as dendritic translation, which involves an uptick in localized protein production within dendrites, the spiny branches that project off the neuron cell body and receive signals from other neurons at synapses. It’s a process key to memory—and its dysfunction is linked to intellectual disorders. Breakthrough in Understanding Memory
That makes the inner workings of dendritic translation a “holy grail for understanding memory formation,” says Rockefeller’s Robert B. Darnell, whose team just published a study in Nature Neuroscience describing a new platform capable of identifying the specific regulatory mechanisms that drive dendritic translation. The team leveraged a method, dubbed TurboID, to discover an entire suite of previously unknown factors in memory formation, revealing now mechanisms that underlie how protein synthesis in dendrites contributes to learning and memory. The findings may also have implications for intellectual disabilities, such as Fragile X syndrome.
“Technological limitations have long prevented a comprehensive inventory of the activity at the synapse involved in memory formation,” says lead author Ezgi Hacisuleyman, who conducted the research as a postdoctoral researcher in Darnell’s laboratory. She is now an assistant professor at The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology. “Our new techniques can accomplish this with extremely high resolution to look at neurons in vitro that are closely mimicking what we see in the brain.”
“Hacisuleyman’s work defines a whole new biochemical pathway which fits with, complements, and vastly expands what we already knew about memory and learning,” adds Darnell, the Robert and Harriet Heilbrunn professor. A Unique Way to Metabolize RNA
Memory formation centers around the hippocampus, a brain region so central to learning that, when surgeons removed it from people with epilepsy in the 1940s, the patients remembered their childhoods but lost the ability to form new memories. It has since become clear that memories form, in part, because of new protein synthesis made locally in the dendrites of the hippocampus.
Darnell, a physician-scientist, observed the importance of dendritic translation firsthand while working with patients whose immune systems had attacked the hippocampus. “I would talk to a patient for 30 minutes, leave the room, walk back in, and it was like they had never seen me before,” he says. “That’s when I began focusing on why neurons of the hippocampus have their own system for regulating RNA metabolism—a system that no other cell in the body uses.”
That system, it turns out, lies at the heart of how our brains form memories and learn new information, and became a focus for the Darnell lab, culminating in his team’s 2003 development of CLIP, a method that allowed researchers to study the proteins that bind and influence RNA. But limitations remained. “Many details about how neurons respond to stimuli at the dendrites were still missing,” Hacisuleyman says. “We needed that information, because that plays a role in determining how neurons function—and where things often go awry in neurologic disease.” Discovering the Micropeptides
To get a better idea of the role that changes in dendrites play in learning, Hacisuleyman extended the TurboID platform to works in concert with RNA-sequencing, CLIP, translation and protein analysis. The platform allowed the team to track activity in dendrites before, during, and several minutes after the neuron activates, capturing the moments critical to protein synthesis in the cell and, more importantly, the stage considered key to memory formation.
An analysis of these crucial moments revealed a microscopic upheaval in the dendrite. Upon activation, local ribosomes jump onto mRNAs, an action that has all the biochemical hallmarks of memory formation, and which models predicted will cause the dendrite to produce not only new proteins, but 1,000 small proteins known as micropeptides, with as-yet unknown function. The team also identified an RNA-binding protein that helps seal the connection between these ribosomes and mRNA, and demonstrated that if that protein is disabled, the proposed micropeptides and their associated downstream proteins will not form.
“We never knew these micropeptides might even exist,” Darnell says. “It opens a new field of study, where we can ask what these peptides might be doing and how they could play into memory formation. It’s such a vast discovery that there are dozens if not hundreds of avenues in which to pursue this.” Future Directions and Implications
Among the many observations that researchers will unpack in future studies, one stood out: the team noted that a certain protein stood out for its prolific binding of mRNA in the dendrite. The protein, called FMRP, is key to brain development and function, and genetic mutations that adversely impact FMRP contribute to Fragile X syndrome, one of the most common genetic causes of intellectual disability. “Our findings fit nicely with the molecular biology of FMRP, and also open the door to future insights into what is going wrong in Fragile X,” Darnell says.
Beyond the paper’s immediate findings, dendritic-TurboID could also allow researchers to examine RNA regulation and protein synthesis in other brain regions and apply the findings to different diseases. “We can now begin to look at many other sites with a fine-toothed comb,” Hacisuleyman says.
“When you develop a new technique as Hacisuleyman did, you enter a room that nobody has ever been in before,” Darnell adds. “The light turns on, and the findings just take your breath away.”
Reference: “Neuronal activity rapidly reprograms dendritic translation via eIF4G2:uORF binding” by Ezgi Hacisuleyman, Caryn R. Hale, Natalie Noble, Ji-dung Luo, John J. Fak, Misa Saito, Jin Chen, Jonathan S. Weissman and Robert B. Darnell, 8 April 2024, Nature Neuroscience .
DOI: 10.1038/s41593-024-01615-5
Neuroscientists Uncover Brain Region ‘Crucial’ to Deep Sleep
Neuroscientists have discovered a surprising new source of deep-sleep brain waves, shaking up our understanding of the architecture of sleep and how we treat sleep disorders.
Our sleep is divided into four main stages, which are determined by the activity of our brain waves. The first stage, N1, is when we first start to fall asleep. At this point, our bodies and brain activities start to slow down. In stage two, our muscles begin to fully relax and our heart rate, breathing, and brain activity continue to slow down. Then, we have deep sleep, which is thought to be the most important stage for body recovery and growth.
Deep sleep is characterized by long, slow brain waves together with short bursts of activity called sleep spindles. Historically, these have been thought to originate from a single brain circuit linking a structure in the middle of the brain, called the thalamus, to the outer cortex. However, a new study from the University of California , Irvine, published in the journal Scientific Reports , suggests that there may be another brain region at play here too. Our sleep is divided into four stages, characterized by different levels of brain activity. “Our research sheds light on a previously unrecognized aspect of deep sleep brain activity,” lead author Mengke Wang, former UC Irvine undergraduate student in biomedical engineering who is now a graduate student at Johns Hopkins University, said in a statement.
“We’ve discovered that the hippocampus, typically associated with memory formation, plays a crucial role in generating slow waves and sleep spindles, offering new insights into how these brain waves support memory processing during sleep.”
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By clicking on SIGN ME UP, you agree to Newsweek’s Terms of Use & Privacy Policy . You may unsubscribe at any time. The role of the hippocampus here adds to previous understanding of the role of deep sleep in memory consolidation, which is thought to continue throughout the final stage of the sleep cycle: REM sleep.
Not only do these results expand understanding of healthy sleep cycles, but they may also offer useful insight into what can go wrong during sleep disorders.
“These findings have significant implications for sleep research, potentially paving the way for new approaches to treating sleep-related disorders,” co-author Gregory Brewer, adjunct professor of biomedical engineering at UC Irvine, said in a statement.
In future studies, the team hopes to explore the therapeutic potential of targeting this hippocampal activity to improve both sleep quality and cognitive function.
Is there a health problem that’s worrying you? Let us know via health@newsweek.com. We can ask experts for advice, and your story could be featured on Newsweek .
Neuroscience study taps into brain network patterns to understand deep focus, attention
Credit: Pixabay/CC0 Public Domain From completing puzzles and playing music, to reading and exercising, growing up Dolly Seeburger loved activities that demanded her full attention. “It was in those times that I felt most content, like I was in the zone,” she remembers. “Hours would pass, but it would feel like minutes.”
While this deep focus state is essential to highly effective work, it’s still not fully understood. Now, a new study led by Seeburger, a graduate student in the School of Psychology, alongside her advisor, Eric Schumacher, a professor in the School of Psychology is unearthing the mechanisms behind it.
The interdisciplinary Georgia Tech team also includes Nan Xu, Sam Larson and Shella Keilholz (Coulter Department of Biomedical Engineering), alongside Marcus Ma (College of Computing), and Christine Godwin (School of Psychology).
The researchers’ study, ” Time-varying functional connectivity predicts fluctuations in sustained attention in a serial tapping task ,” published in Cognitive, Affective, and Behavioral Neuroscience , investigates brain activity via fMRI during periods of deep focus and less-focused work.
The work is the first to investigate low-frequency fluctuations between different networks in the brain during focus, and could act as a springboard to study more complex behaviors and focus states.
“Your brain is dynamic. Nothing is just on or off,” Seeburger explains. “This is the phenomenon we wanted to study. How does one get into the zone? Why is it that some people can sustain their attention better than others? Is this something that can be trained? If so, can we help people get better at it?” The dynamic brain
The team’s work is also the first to study the relationship between fluctuations in attention and the brain network patterns within these low-frequency 20-second cycles.
“For quite a while, the studies on neural oscillations focused on faster temporal frequencies, and the appreciation of these very low-frequency oscillations is relatively new,” Seeburger says. “But, these low-frequency fluctuations may play a key role in regulating higher cognition such as sustained attention.”
“One of the things we’ve discovered in previous research is that there’s a natural fluctuation in activity in certain brain networks. When a subject is not doing a specific task while in the MRI scanner, we see that fluctuation happen roughly every 20 seconds,” adds co-author Schumacher, explaining that the team was interested in the pattern because it is quasi-periodic, meaning that it doesn’t repeat exactly every 20 seconds, and it varies between different trials and subjects.
By studying these quasi-periodic cycles, the team hoped to measure the relationship between the brain fluctuation in these networks and the behavioral fluctuation associated with changes in attention. Your attention needed
To measure attention, participants tapped along to a metronome while in an fMRI scanner. The team could measure how “in the zone” participants were by measuring how much variability was in each participant’s taps—more variability suggested the participant was less focused, while precise tapping suggested the participant was “in the zone.”
The researchers found that when a subject’s focus level changed, different regions of the brain synchronized and desynchronized, in particular the fronto-parietal control network (FPCN) and default mode network (DMN), The FPCN is engaged when a person is trying to stay on task, whereas the DMN is correlated with internally-oriented thoughts (which a participant might be having when less focused).
“When one is out-of-the-zone, these two networks synchronize, and are in phase in the low frequency,” Seeburger explains. “When one is in the zone, these networks desynchronize.”
The results suggest that the 20-second patterns could help predict if a person is sustaining their attention or not, and could provide key insight for researchers developing tools and techniques that help us deeply focus. The big picture
While the direct relationship between behavior and brain activity is still unknown, these 20-second patterns in brain fluctuation are seen universally, and across species.
“If you put someone in a scanner and their mind is wandering, you find these fluctuations. You can find these quasi-period patterns in rodents. You can find it in primates,” Schumacher says. “There’s something fundamental about this brain network activity.”
“I think it answers a really fundamental question about the relationship between behavior and brain activity ,” he adds. “Understanding how these brain networks work together and impact behavior could lead to new therapies to help people organize their brain networks in the most efficient way.”
And while this simple task might not investigate complex behaviors, the study could act as a springboard to move into more complicated behaviors and focus states.
“Next, I would like to study sustained attention in a more naturalistic way,” Seeburger says. “I hope that we can further the understanding of attention and help people get a better handle on their ability to control, sustain, and increase it.”
More information: Dolly T. Seeburger et al, Time-varying functional connectivity predicts fluctuations in sustained attention in a serial tapping task, Cognitive, Affective, & Behavioral Neuroscience (2024). DOI: 10.3758/s13415-024-01156-1
Provided by Georgia Institute of Technology
Opinion: Brain imaging has promise to improve mental health treatment for kids. Here’s why.
Brain imaging in a child. (Jillian Lee Wiggins ) Wiggins is an associate professor of psychology at San Diego State University, and lives in Hillcrest. She will delve further into this topic at the TEDxSan Diego CommUNITY speaker series on Wednesday at the David & Dorothea Garfield Theatre in La Jolla. Speakers start at 7 p.m.
Right now, we are fighting for the future of our children’s mental health. The U.S. surgeon general has declared a youth mental health crisis, and this has only gotten worse with the pandemic. We have a huge barrier to solving this crisis, though. Typically, when parents bring their children to the doctor’s office for anxiety or depression, a psychologist or psychiatrist typically try, through trial and error, a laundry list of potential treatments until something works.
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This approach is really inefficient, and costly, and grinds down children and parents every time a treatment doesn’t work. And it’s not because the doctors are trying to be obtuse — they just can’t yet look under the hood, into the child’s brain, to see what is wrong and figure out which kids will need what treatment.
I am the director of San Diego State University’s Translational Emotion Neuroscience and Development (TEND) Lab . I am on the vanguard of a scientific movement to address this youth mental health crisis by leveraging brain imaging.
You might be familiar with a traditional MRI, where they take a static image of your brain, which can be compared to looking under the hood of the car while the car is off.
At the TEND lab, we use a special form of brain imaging, functional MRI, to look “under the hood” in a way that is completely beyond just a static image. When children come into our lab, they lie in the MRI and play specially designed video games that tap psychological processes like how they feel when they win or lose money, how they react to people being angry or happy with them, and what it’s like when they’re frustrated. In functional MRI, the images are dynamic, and we get to see the brain activation in response to these emotional events.
Through this work, we’re now able to look under the hood while the car is running to identify what kind of brain signatures predict which children will get better after established psychological treatments, and whether we discover the brain signatures that will help us predict, in advance, which children are just experiencing mild emotional problems that will pass and get better on their own. Once we know those brain mechanisms of the risk for mental health problems, we can target them for novel, innovative preventive interventions and new, personalized treatments.
One of the best, evidence-based treatments out there is called Trauma Focused Cognitive Behavioral Therapy, or TF-CBT. In TF-CBT, children talk through their experiences with a therapist and learn how to calm themselves and cope. Even though people on average get better after TF-CBT, for about a third of people, it doesn’t work. So, we had to find out what was different in the brains of children who did get better versus those who did not.
What we found is that the children who did not get better had something in common: the way their brains reacted to getting rewards and being denied a reward. Further, we found that children who ended up not getting better after trauma treatment had brains that reacted totally inappropriately to getting a reward and being denied a reward. They showed the opposite patterns of activation compared to children who ended up getting better. This indicates that some fundamental problems with how these children’s brains value and react to rewards might be preventing them from healing from their trauma.
As researchers, this is an exciting time. We are just beginning to peek under the hood to find out how the brain works, and we are now working on larger studies to make sure that we can replicate and expand our findings. Imagine a future where, instead of trying treatments until something works — a doctor will order a lab test based on an MRI of the child’s brain. And, from the results of that lab test, they will prescribe a personalized treatment for that child.
When scientists were studying electricity centuries ago, they could have never imagined that their work would lead to the cell phones, computers and technology that we have today. Similarly, I will probably never live to see the full impact of my work, but my team and I are building the road to a better mental health future for our children.
Blended antioxidant supplement may help boost memory and cognition
New research links a blend of antioxidants to improved cognition, at least in mice. Lilith Matevosyan/Stocksy A new study from Japan has shown that blended antioxidants may improve cognition and memory while suppressing age-related muscle decline in mice.
The antioxidant blend used in the study was supplied by a supplement marketed in Japan.
However, experts do not recommend inventing one’s own blended antioxidants by combining supplements, as such at-home experiments may be dangerous.
Cognitive benefits from blended antioxidants have been observed in mouse research, but, so far, there have not been significant human studies of their effects.
A new study in mice finds that supplements containing a blend of antioxidants may improve spatial cognition, short-term memory, and — surprisingly — muscle durability in older mice.
Antioxidants help promote the health of cells by reducing an excess of unstable free radical molecules that can damage healthy cells. While free radicals occur naturally, too many of them can overwhelm healthy cells, causing what’s called oxidative stress . Oxidative stress has been linked to a wide range of health issues.
Antioxidants are molecules that can help inhibit or prevent cell damage in the body. They are often found in plants, and some occur in the human body, although there are also synthetic antioxidants consumed as supplements.
The researchers in Japan used a blended antioxidant product, Twendee X, a product currently marketed in that country. It contains eight different types of antioxidants and was formulated by Professor Haruhiko Inufusa of the Department of Antioxidant Research, Center for Scientific Research and Innovation at Gifu University in Japan.
For the new study, 18-month-old genetically modified mice were given a blended antioxidant in water that they were allowed to drink or not drink at will for a month.
Their spatial cognition and short-term memory improved during the test period, as measured by their success in a Morris water maze and Y-maze , compared to mice in the control group provided plain filtered tap water.
Treadmill tests showed that by the end of the study, the blended antioxidant mice increased their running distance significantly more than their normal, control counterparts who were not taking blended antioxidants.
Further attempts to train mice on the treadmills with additional supplement administration showed no discernible effects between the two groups, suggesting the blended antioxidant may not improve exercise capacity or strength, but may help prevent age-related muscle decline.
In post-mortem examination of the blended-antioxidant mice’s brains, the researchers observed a significant decrease in aspartate aminotransferase — an enzyme indicating muscle damage — alanine aminotransferase , as well as total cholesterol values.
The study is published in MDPI . Can you make blended antioxidants at home?
Blended antioxidants are supplements in which multiple antioxidants have been combined. Their purported benefit is the strengthening of cognition. There have been several studies investigating their value, but as Michelle Routhenstein , registered dietician and nutritionist at EntirelyNourished.com noted, clinical studies have occurred only with mice so far.
When asked if blended antioxidants are safe, the study’s first author, Kouji Fukui, PhD , pointed out simply that “This blended supplement is already on sale. Anyone can purchase it. I also drink it every day.”
Both Fukui and Routhenstein cautioned against concocting one’s own blend of antioxidants from existing supplements, although “a combination of them produces a higher effect than a single one,” said Fukui.
“It is nearly impossible for general consumers to choose multiple supplements and continue taking them. Excessive intake of some vitamins can be a problem,” said Fukui. He noted that TwendeeX also “contains amino acids in addition to vitamins, which I think is an interesting combination.”
Routhenstein agreed, saying, “There are safety concerns regarding homemade antioxidant blends, such as challenges in ensuring accurate dosage, potential interactions with medications, contamination, and the risk of toxicity, especially with fat-soluble antioxidants, due to excessive intake.”
Routhenstein said, however, “for research purposes, it is easier to assess [blended antioxidants’] effect and compliance when formulated in specific doses and given in a clinically controlled and studied procedure.” Can I get these antioxidants from foods?
A person can safely replicate the blended effect by eating a combination of foods that contain different antioxidants.
Antioxidants are readily available in various healthy foods. Among these are broccoli , carrots , potatoes, and sweet potatoes .
Cabbage, lettuce, asparagus , and squash are also great sources. Blueberries, strawberries , pecans, artichokes , kale, raspberries , spinach , and okra are also rich in antioxidants, as are beets , beans , and dark chocolate. Antioxidants aid strength in aging muscles
In studies, antioxidants have been repeatedly found to support cognition, and, thus, the study’s finding that spatial memory and short-term memory benefited from blended antioxidants is not unexpected, at least in mice.
However, Fukui expressed surprise at his study’s finding that they also seemed to suppress an age-related decline in muscle strength.
“Muscle strength declines with aging, but our blended supplement prevents this decline,” he said. Fukui pointed out that aging is associated with frailty and sarcopenia, so the finding may have to do with the [ Coenzyme Q10 ] and amino acid ingredients in TwendeeX. “This may have had a positive effect on mitochondria and muscle tissue,” he said. Although the findings are promising, it is also too early to generalize the results for humans.“Antioxidants may help alleviate exercise-induced oxidative stress in muscles, potentially aiding in recovery, which can help strengthen muscles. However, more research is necessary to verify these effects of blended antioxidants in human trials,” Routhenstein said. How blended antioxidants may help brain fog One of the symptoms associated with long COVID is “brain fog,” a dulling of cognitive powers that can result in a significant change in one’s quality of life.“It has been suggested that [blended antioxidants] may also be effective against the aftereffects of coronavirus. The main premise is that they have an antioxidant effect,” Fukui added.
NeuM technology revolutionizes neuron labeling for neurodegenerative disease research
Alzheimer’s disease and Parkinson’s disease, along with stroke, are among the top three neurodegenerative disorders, characterized by the malfunction and progressive degeneration of neurons, the nerve cells. Understanding the mechanisms underlying these neurological disorders and developing therapies requires labeling technologies that can visualize neuronal changes not only in normal conditions but also in disease states.
A research team led by Dr. Kim Yun Kyung from the Brain Science Institute at the Korea Institute of Science and Technology (KIST), in collaboration with Professor Chang Young-Tae’s team from Pohang University of Science and Technology, has announced the development of a next-generation neuron labeling technology called NeuM. NeuM (Neuronal Membrane-selective) selectively labels neuronal membranes, visualizing neuronal structures and allowing real-time monitoring of neuronal changes.
Neurons continuously modify their structure and function to transmit information from sensory organs to the brain, regulating thoughts, memories, and behaviors. Therefore, to overcome degenerative neurological diseases, it is essential to develop techniques that selectively label living neurons for real-time monitoring. However, current gene-based and antibody-based labeling technologies, commonly used to observe neurons, suffer from low accuracy and difficulty in long-term tracking due to their dependence on specific gene expression or proteins.
NeuM, developed by the research team through molecular design of neuronal cells, possesses excellent binding affinity to neuronal membranes, enabling long-term tracking and high-resolution imaging of neurons. The fluorescent probes within NeuM bind to neuronal membranes utilizing the activity of living cells, emitting fluorescent signals upon excitation by specific wavelengths of light. This visualization of neuronal membranes allows for detailed observation of neuronal terminal structures and high-resolution monitoring of neuronal differentiation and interactions.
NeuM, as the first technology to stain cell membranes through endocytosis in living neurons, exhibits selective reactivity towards living cells, excluding dead cells without internalization. Moreover, the research team has succeeded in extending the observation time of neurons from a mere 6 hours to up to 72 hours, enabling the capture of dynamic changes in living neurons over an extended period in response to environmental changes.
NeuM is expected to provide insights into research and therapy development for degenerative neurological diseases, for which there are currently no cures. These diseases, including Alzheimer’s, result from neuronal damage due to the production of toxic proteins such as amyloid and the influx of inflammatory substances. NeuM’s precise observation of neuronal changes can effectively facilitate the evaluation of candidate therapeutic compounds. NeuM, developed this time, can distinguish aging and degenerating neurons, becoming a crucial tool in elucidating the mechanisms of degenerative brain disorders and developing treatments.” He further added, “In the future, we plan to refine NeuM for even more precise analysis of neurons by designing fluorescence wavelengths to distinguish colors such as green and red.” Dr. Kim Yun Kyung, Brain Science Institute, Korea Institute of Science and Technology KIST was established in 1966 as the first government-funded research institute in Korea. KIST now strives to solve national and social challenges and secure growth engines through leading and innovative research. For more information, please visit KIST’s website at https://eng.kist.re.kr/
This research was supported by the Ministry of Science and ICT (Minister Lee Jong-ho) through KIST’s major projects and the Dementia Overcoming Project (RS-2023-00261784). The research results have been published in the latest issue of the international academic journal “Angewandte Chemie.”
Source:
National Research Council of Science & Technology
Journal reference:
Sung, Y., et al . (2023). NeuM: A Neuon‐Selective Probe Incorporates into Live Neuronal Membranes via Enhanced Cathrin‐Mediated Endocytosis in Primary Neurons. Angewandte Chemie . doi.org/10.1002/anie.202312942 .
Study questions benefits of brain stimulation for memory improvement
Credit: Unsplash+. Researchers at the University of Sheffield have raised doubts about the effectiveness of non-invasive brain stimulation methods, such as transcranial direct current stimulation (tDCS), for enhancing visual working memory.
Their findings, published in Communications Psychology, challenge previous optimistic reports and underscore the need for careful scrutiny of such brain stimulation techniques.
Visual working memory plays a vital role in our cognitive system, enabling us to hold and process visual information temporarily.
This ability is crucial for everyday tasks and is affected by aging and diseases like Alzheimer’s.
Consequently, scientists have been keen on finding ways to bolster working memory, with brain stimulation emerging as a notable area of interest over the past two decades.
tDCS, a low-cost and easy-to-use technique often compared to the TENS machines used for back pain, has been highlighted in some studies for its potential to improve various psychological functions, including memory and socialization.
It has even been incorporated into guidelines for treating conditions such as depression, based on its purported benefits following multiple sessions.
However, the University of Sheffield’s recent study, led by Dr. Shuangke Jiang along with Dr. Myles Jones and Dr. Claudia von Bastian from the Department of Psychology, aimed to replicate one particularly high-profile study that claimed significant improvements in working memory from brief tDCS sessions.
The team employed enhanced methodology but found strong evidence contradicting the claimed benefits of tDCS on working memory enhancement from a single 15-minute session.
Dr. Jiang stated, “We have replicated this study with improved methodology and found unequivocal evidence that tDCS does not improve working memory.”
This conclusion not only casts doubt on the efficacy of tDCS for memory improvement but also highlights the broader issue of replicability in psychological research.
The study underscores the importance of replication to build a reliable and informative evidence base regarding the true effects of cognitive enhancement interventions.
This development is a reminder of the complexities involved in brain research and the necessity of rigorous testing and validation of cognitive enhancement techniques.
As the scientific community continues to explore the potential of brain stimulation, this study contributes to a more nuanced understanding of its limitations and the critical need for replication in psychological research.
If you care about brain health, please read studies about how the Mediterranean diet could protect your brain health, and blueberry supplements may prevent cognitive decline.
For more information about brain health, please see recent studies about antioxidants that could help reduce dementia risk , and Coconut oil could help improve cognitive function in Alzheimer’s .
The research findings can be found in Communications Psychology.
Copyright © 2024 Knowridge Science Report . All rights reserved.
Dartmouth-led research identifies unique brain areas for emotion regulation
Ever want to scream during a particularly bad day, but then manage not to? Thank the human brain and how it regulates emotions, which can be critical for navigating everyday life. As we perceive events unfolding around us, the ability to be flexible and reframe a situation impacts not only how we feel, but also our behavior and decision-making.
In fact, some of the problems associated with mental health relate to individuals’ inability to be flexible, such as when persistent negative thoughts make it hard to perceive a situation differently.
To help address such issues, a new Dartmouth-led study is among the first of its kind to separate activity relating to emotion generation from emotion regulation in the human brain. The findings are published in Nature Neuroscience . As a former biomedical engineer, it was exciting to identify some brain regions that are purely unique to regulating emotions. Our results provide new insight into how emotion regulation works by identifying targets which could have clinical applications.” Ke Bo, lead author, postdoctoral researcher in the Cognitive and Affective Neuroscience Lab (CANlab) at Dartmouth For example, the systems the researchers identified could be good targets for brain stimulation to enhance the regulation of emotion.
Using computational methods, the researchers examined two independent datasets of fMRI studies obtained earlier by co-author Peter Gianaros at the University of Pittsburgh. Participants’ brain activity was recorded in an fMRI scanner as they viewed images that were likely to draw a negative reaction such as a bloody scene or scary- looking animals.
The participants were then asked to recontextualize the stimulus by generating new kinds of thoughts about an image to make it less aversive, before a neutral image was presented followed by another dislikable image.
By examining the neural activity, researchers could identify the brain areas that are more active when emotions are regulated versus when emotions are generated.
The new study reveals that emotion regulation, also known in neuroscience as “reappraisal,” involves particular areas of the anterior prefrontal cortex and other higher-level cortical hierarchies whose role in emotion regulation had not previously been isolated with this level of precision. These regions are involved in other high-level cognitive functions and are important for abstract thought and long-term representations of the future.
The more people are able to activate these emotion regulation-selective brain regions, the more resilient they are to experiencing something negative without letting it affect them personally. These findings build on other research linking these areas to better mental health and the ability to resist temptations and avoid drug addiction.
The results also demonstrated that the amygdala, which is known as the threat-related brain region responsible for negative emotion and has long been considered an ancient subcortical threat center, responds to aversive experiences the same way, whether people are using their thoughts to self-regulate down-regulate negative emotion or not. “It’s really the cortex that is responsible for generating people’s emotional responses, by changing the way we see and attach meaning to events in our environments,” says Bo.
The researchers were also interested in identifying the neurochemicals that interact with emotion regulation systems. Neurotransmitters like dopamine and serotonin shape how networks of neurons communicate and are targets for both illicit drugs and therapeutic treatments alike. Some neurotransmitters may be important for enabling the ability to self-regulate or “down-regulate.”
The team compared the emotion regulation brain maps from the two datasets to neurotransmitter binding maps from 36 other studies. The systems involved in regulating negative emotion overlapped with particular neurotransmitter systems.
“Our results showed that receptors for cannabinoids, opioids, and serotonin, including 5H2A, were especially rich in areas that are involved in emotion regulation,” says senior author Tor Wager, the Diana L. Taylor Distinguished Professor in Neuroscience and director of the Dartmouth Brain Imaging Center at Dartmouth. “When drugs that bind to these receptors are taken, they are preferentially affecting the emotion regulation system, which raises questions about their potential for long-term effects on our capacity to self-regulate.”
Serotonin is well-known for its role in depression, as the most widely used antidepressant drugs inhibit its reuptake in synapses, which transmit signals from one neuron to another.
5H2A is the serotonin receptor most strongly affected by another exciting new type of treatment for mental health – psychedelic drugs. The study’s findings suggest that the effects of drugs on depression and other mental health disorders may work in part by altering how we think about life events and our ability to self-regulate. This may help explain why drugs, particularly psychedelics, are likely to be ineffective without the right kind of psychological support. The study could help improve therapeutic approaches by increasing our understanding of why and how psychological and pharmaceutical approaches need to be combined into integrated treatments.
“It’s important to consider these types of connections that come from basic science,” says Wager. “Understanding drug effects requires understanding the brain systems involved and what they’re doing at a cognitive level.”
Bo (Ke.Bo@dartmouth.edu) and Wager (Tor.D.Wager@dartmouth.edu) are available for comment. CANlab members Mijin Kwon, Guarini ’24 and Michael Sun, a postdoctoral researcher at Dartmouth, and Thomas Kraynak at the University of Pittsburgh also contributed to the study.
Source:
Dartmouth College
Journal reference:
Bo, K., et al. (2024). A systems identification approach using Bayes factors to deconstruct the brain bases of emotion regulation. Nature Neuroscience . doi.org/10.1038/s41593-024-01605-7 .
6 Mushrooms you can eat to prevent cognitive impairment and reduce your dementia risk
A recent study by researchers at the National University of Singapore (NUS) found that older adults who consume more mushrooms in their diet have a significantly lower risk of mild cognitive impairment than those who don’t.
Mild cognitive impairment is a condition defined by experts as the stage between the expected cognitive decline that occurs with age and the more serious decline caused by dementia . While mild cognitive impairment could increase an adult’s risk of developing Alzheimer’s disease , this condition can be prevented or treated with healthy lifestyle adjustments and dietary interventions.
According to research, there is no single cause of mild cognitive impairment, but certain changes in the structure of the brain are often observed in people with this condition. These same changes can also be seen in the brains of people with Alzheimer’s or other forms of dementia, albeit in a worse degree. Suffering from diabetes, stroke or depression is said to increase a person’s likelihood of developing mild cognitive impairment .
Although the symptoms of mild cognitive impairment are not as severe as those of Alzheimer’s or dementia, the condition can still impact quality of life. Common signs of mild cognitive impairment include being forgetful, having trouble coming up with words and losing things often. But unlike people with Alzheimer’s, those suffering from mild cognitive impairment do not experience personality changes and can still perform their daily activities by themselves. A mushroom-rich diet can help prevent mild cognitive impairment
To understand how mushroom intake can affect brain function, the NUS researchers analyzed data from 663 Singaporeans aged 60 and above. This six-year study, published in the Journal of Alzheimer’s Disease , was conducted from 2011 to 2017 and looked in particular at the amount of mushrooms the participants consumed in a week.
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The researchers found that compared to participants who ate mushrooms less than once a week, those who consumed more than two portions of mushrooms per week had a 50 percent lower risk of having mild cognitive impairment. This association was independent of age, gender, education, alcohol consumption, smoking habits, physical and social activities, and other conditions like hypertension, stroke, diabetes and heart disease.
For reference, a portion is equivalent to a 3/4 cup serving of cooked mushrooms weighing about 150 grams (g). Two portions is about half a plate of cooked mushrooms. This is how much you should eat in a week to decrease your odds of having mild cognitive impairment, according to the study. On the other hand, the study also reported that consuming even just one small portion of mushrooms weekly can go a long way toward keeping your brain healthy.
Mushrooms are a versatile and nutritious culinary ingredient, being one of the few food sources of ergosterol . This compound is converted into vitamin D2 upon exposure to ultraviolet (UV) light. A one cup serving of mushrooms can also provide plenty of other nutrients , such as protein, copper, B vitamins, potassium and iron.
But most importantly, the NUS researchers believe that the brain-boosting effect of mushrooms is thanks to ergothioneine, an amino acid found in almost all mushroom varieties. “[Ergothioneine] is a unique antioxidant and anti-inflammatory which humans are unable to synthesise on their own. But it can be obtained from dietary sources, one of the main ones being mushrooms,” explained Dr. Irwin Cheah, one of the study authors.
According to a more recent study published FEBS Letters , ergothioneine has shown antidepressant activities in mice and memory-enhancing effects in humans . Its brain benefits can be attributed to its ability to protect brain cells (neurons) from oxidative damage and promote neurogenesis (formation of new neurons) and neuronal maturation.
Other bioactive compounds in mushrooms, such as hericenones, erinacines, scabronines and dictyophorines, can also promote the synthesis of neuronal growth factors and may also help reduce your risk of cognitive decline. (Related: Organic functional mushrooms: best immune-boosting medicine from Mother Nature ) 6 Brain-supporting mushrooms to incorporate into your meals
If you’re wondering which among the 200 edible mushrooms known to humans you should add to your diet for better brain health, here are six of the best ones at supporting healthy brain function, according to science. Chaga mushroom ( Inonotus obliquus )
According to a study published in the International Journal of Biological Macromolecules , chaga mushroom contains a bioactive polysaccharide that can protect against Alzheimer’s disease by enhancing the expression of Nrf2 in the brain. Nrf2 is the protein ” responsible for regulating an extensive panel of antioxidant enzymes” which are involved in detoxification and combating oxidative stress.
The brain’s susceptibility to oxidative stress is a crucial detrimental factor in Alzheimer’s disease . (Related: Here’s all you need to know about chaga mushrooms and their health benefits .) Oyster mushroom ( Pleurotus ostreatus )
Widely used in Traditional Chinese Medicine (TCM), the oyster mushroom is often prescribed to help relax the muscles, tendons and joints. Research has found that, like chaga, the oyster mushroom can help decrease oxidative stress in the brain .
According to a study by Indian researchers, oyster mushrooms contain compounds that can protect against oxidative damage by elevating the levels of antioxidants , such as vitamin C and glutathione, and various antioxidant enzymes in the brain in response to stressors. Lion’s mane ( Hericium erinaceus )
When it comes to supporting a healthy brain and nervous system, lion’s mane is considered one of the best mushrooms to eat. Studies show that the hericenones and erinacines in lion’s mane can induce the expression of nerve growth factors that help regulate the growth, development and maintenance of brain neurons.
A clinical study involving Japanese adults with mild cognitive impairment also found that other components in lion’s mane, particularly in its fruiting body where hericenones are concentrated, […]