Brain capillary structures show a correlation with their neuron structures — ScienceDaily


Drs. Itokawa, Mizutani and colleagues performed microtomography experiments the BL20XU beamline of the SPring-8 synchrotron radiation facility and found that brain capillary structures show a correlation with their neuron structures.

Brain blood vessels constitute a micrometer-scale vascular network responsible for supply of oxygen and nutrition. In this study, we analyzed cerebral tissues of the anterior cingulate cortex and superior temporal gyrus of schizophrenia cases and age/gender-matched controls by using synchrotron radiation microtomography or micro-CT in order to examine the three-dimensional structure of cerebral vessels.

All post-mortem human cerebral tissues were collected with informed consent from the legal next of kin using protocols approved by the Clinical Study Reviewing Board of Tokai University School of Medicine (application no. 07R-018) and the Ethics Committee of Tokyo Metropolitan Institute of Medical Science (approval no. 17-18). This study was conducted according to the Declaration of Helsinki under the approval of the Ethics Committee for the Human Subject Study of Tokai University (approval nos. 11060, 11114, 12114, 13105, 14128, 15129, 16157, 18012, 19001, 20021, and 20022). The schizophrenia patients S1-S4 and control cases N1-N4 of this study are the same as those analyzed in our previous report on neuron structure. Cerebral tissues of Brodmann area 22 (BA22) of the superior temporal gyrus and BA24 of the anterior cingulate cortex were collected from the left hemispheres of the post-mortem brains and subjected to Golgi impregnation. The Golgi-stained tissues were then embedded in borosilicate glass capillaries using epoxy resin.

Three-dimensional structures of blood vessel networks in the brain tissues of BA22 of the superior temporal gyrus and BA24 of the anterior cingulate cortex were visualized by using synchrotron radiation microtomography or micro-CT. Over 1 m of cerebral blood vessels was traced to build Cartesian-coordinate models, which were then used for calculating structural parameters including the diameter and curvature of the vessels.

The curvature plot illustrates a significant correlation of the mean curvature of capillary vessels to that of neurites (Spearman’s ρ = 0.63, p = 0.011, n = 16), indicating that the brain tissues with tortuous neuronal networks have tortuous capillary vessels. No significant difference in the slope was observed between the schizophrenia and control groups. The mean capillary curvature showed a difference in its variance between brain areas. The capillary curvatures of BA22 were widely distributed, while those of BA24 were limited to a confined range, resulting in a significant difference in variance (p = 0.019, Bartlett’s test, n = 8). We also examined the relation between the capillary diameter and neurite thickness radius. In contrast to the curvature correlation, the mean capillary diameter showed no correlation with the neurite thickness radius, but was rather constant regardless of neurite thickness. This result indicates that the capillary vessel size is determined independently of the neuron structure.

Our previous studies indicated that the neurites of schizophrenia cases are thin and tortuous compared to controls. The curved capillaries with a constant diameter should occupy a nearly constant volume, while neurons suffering from neurite thinning should have reduced volumes, resulting in a volumetric imbalance between the neurons and the vessels. We suggest that the observed structural correlation between neurons and blood vessels is related to neurovascular abnormalities in schizophrenia.

Kraepelin placed schizophrenia in a chapter on metabolic disorders in the fifth edition of his Psychiatrie published in 1896. He predicted metabolic disfunction and neuropathological change as the basis of schizophrenia. we can regard the above-mentioned results as the first example suggesting metabolic abnormality due to capillary and neuron imbalance.

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Q&A: Brain food in a bottle


This week we speak to Angus Brown, founder of Ārepa. Dubbed “the worlds smartest drink”, the caffeine-free product is scientifically proven to keep you feeling calm and thinking clear under moments of pressure. By the end of 2020, the brand sold more than a million units and from March has been available as a new functional beverage category at Coles focusing on brain health and mental wellbeing.

ISB: What was the inspiration behind you developing Ārepa?

AB: I was inspired to develop Ārepa after losing a friend to mental health and grandparents to cognitive-related illnesses, at the time I was in my first job out of university working for a very large energy drink company in sales and thought, “Am I doing any good here?” Our mission now is to make brains work better through accessible and proven brain food.

ISB: What was the biggest challenge you faced getting the enterprise off the ground and how did you overcome it?

AB: Convincing a world-renowned Australian neuroscientist to help us develop a brain drink and then convincing investors to back us heading into our first clinical trial. These things are high risk but we believe it has paid off as we have the published evidence and a growing number of happy customers who feel the effects.

ISB: How have you approached persuading the market about the product’s health benefits bearing in mind scepticism around false marketing behind other “so-called” health products?

AB: We knew this would be our biggest challenge upfront so that’s why we brought on Australias top neuroscientist Professor Andrew Schloly to help with the formulation and research. We then worked with independent universities to validate the effects in the beverage to ensure that the finished product worked (which it did!). We now have over $3 million of clinical trials deployed across seven different independent studies exploring how our formula affects aspects of mental performance and long-term neurological health to help build out the dossier of evidence towards Ārepa as a natural brainfood backed by science.

ISB: And how did you go about getting the range into 200 stores of the country’s largest supermarket chain?

AB: Coles were great to work with, they could see the science and our proof of sales and success in New Zealand. We are stoked to be ranged with them and are working hard to educate Australians on why a caffeine-free brain drink might be a smarter alternative under moments of pressure or stress.

ISB: What is your vision for the development of the business in the next couple of years?

AB: Our mission is to make brains work better and delay the onset of neurological decline worldwide through accessible, sustainable and proven brain food. We have a large study getting set up looking into the neuroprotective effects of our formula, if we show an effect and get more products like this into the hands of Australians we can impart a benefit to them and reduce the economic burden on the country.

ISB: And, finally, what is the number one lesson you’ve learnt on your journey you’d share with others looking to start their own business?

AB: Find smart people who know the industry to advise you, work hard and never give up!



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It is the first work to show that sonothermogenetics can control behavior by stimulating a specific target deep in the brain — ScienceDaily


Neurological disorders such as Parkinson’s disease and epilepsy have had some treatment success with deep brain stimulation, but those require surgical device implantation. A multidisciplinary team at Washington University in St. Louis has developed a new brain stimulation technique using focused ultrasound that is able to turn specific types of neurons in the brain on and off and precisely control motor activity without surgical device implantation.

The team, led by Hong Chen, assistant professor of biomedical engineering in the McKelvey School of Engineering and of radiation oncology at the School of Medicine, is the first to provide direct evidence showing noninvasive, cell-type-specific activation of neurons in the brain of mammal by combining ultrasound-induced heating effect and genetics, which they have named sonothermogenetics. It is also the first work to show that the ultrasound- genetics combination can robustly control behavior by stimulating a specific target deep in the brain.

Results of the three years of research, which was funded in part by the National Institutes of Health’s BRAIN Initiative, were published online in Brain Stimulation May 11, 2021.

The senior research team included experts from both the McKelvey School of Engineering and the School of Medicine, including Jianmin Cui, professor of biomedical engineering; Joseph P. Culver, professor of radiology, of physics and of biomedical engineering; Mark J. Miller, associate professor of medicine in the Division of Infectious Diseases in the Department of Medicine; and Michael Bruchas, formerly of Washington University, now professor of anesthesiology and pharmacology at the University of Washington.

“Our work provided evidence that sonothermogenetics evokes behavioral responses in freely moving mice while targeting a deep brain site,” Chen said. “Sonothermogenetics has the potential to transform our approaches for neuroscience research and uncover new methods to understand and treat human brain disorders.”

Using a mouse model, Chen and the team delivered a viral construct containing TRPV1 ion channels to genetically-selected neurons. Then, they delivered small burst of heat via low-intensity focused ultrasound to the select neurons in the brain via a wearable device. The heat, only a few degrees warmer than body temperature, activated the TRPV1 ion channel, which acted as a switch to turn the neurons on or off.

“We can move the ultrasound device worn on the head of free-moving mice around to target different locations in the whole brain,” said Yaoheng Yang, first author of the paper and a graduate student in biomedical engineering. “Because it is noninvasive, this technique has the potential to be scaled up to large animals and potentially humans in the future.”

The work builds on research conducted in Cui’s lab that was published in Scientific Reports in 2016. Cui and his team found for the first time that ultrasound alone can influence ion channel activity and could lead to new and noninvasive ways to control the activity of specific cells. In their work, they found that focused ultrasound modulated the currents flowing through the ion channels on average by up to 23%, depending on channel and stimulus intensity. Following this work, researchers found close to 10 ion channels with this capability, but all of them are mechanosensitive, not thermosensitive.

The work also builds on the concept of optogenetics, the combination of the targeted expression of light-sensitive ion channels and the precise delivery of light to stimulate neurons deep in the brain. While optogenetics has increased discovery of new neural circuits, it is limited in penetration depth due to light scattering and requires surgical implantation of optical fibers.

Sonothermogenetics has the promise to target any location in the mouse brain with millimeter-scale resolution without causing any damage to the brain, Chen said. She and the team continue to optimize the technique and further validate their findings.

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A brain cancer diagnosis can be overwhelming, but one survivor is using her experience to help others


The diagnosis that came back was very different.

“I went in in the morning thinking I had sinusitis, and I walked home that afternoon with brain cancer,” Ms Bennett said.

Although the severity of the diagnosis didn’t immediately sink in, the mother of two soon found herself in a flurry of appointments, specialists and confusing information.

Feeling scared and lost, Ms Bennett started thinking of a way to make the news of a brain cancer diagnosis easier to deal with.

This month she launched The Survivorship Diary: the first resource in Australia dedicated to guiding brain cancer patients through the treatment.

“This diary is my attempt to help people manage the barrage of information after receiving their diagnosis,” she said.

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Any alcohol causes damage to the brain, study finds : Health


I don’t know why this is a surprise. At least if you drink enough to get drunk, the function of the brain is temporarily affected; it would amaze me if it could be true that an affected neuron returns to the exact same level.

I have limited experience with being drunk, a little more experience with weed where I became non-functional (like taking a whiz was a challenge and speaking was somehow difficult) and I sure wondered how much function I lost permanently after such an episode.

Have said the above, perhaps there are drugs that temporarily affect brain cells — interfere with neurotransmitters or simulate them but are not neurotoxic. But I think in vitro, alcohol kills neurons and therefore it is to me a scary thing to imbibe.

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Damage to white matter is linked to worse cognitive outcomes after brain injury — ScienceDaily


A new University of Iowa study challenges the idea that gray matter (the neurons that form the cerebral cortex) is more important than white matter (the myelin covered axons that physically connect neuronal regions) when it comes to cognitive health and function. The findings may help neurologists better predict the long-term effects of strokes and other forms of traumatic brain injury.

“The most unexpected aspect of our findings was that damage to gray matter hubs of the brain that are really interconnected with other regions didn’t really tell us much about how poorly people would do on cognitive tests after brain damage. On the other hand, people with damage to the densest white matter connections did much worse on those tests,” explains Justin Reber, PhD, a UI postdoctoral research fellow in psychology and first author on the study. “This is important because both scientists and clinicians often focus almost exclusively on the role of gray matter. This study is a reminder that connections between brain regions might matter just as much as those regions themselves, if not more so.”

The new study, published in PNAS, analyzes brain scans and cognitive function tests from over 500 people with localized areas of brain damage caused by strokes or other forms of brain injury. Looking at the location of the brain damage, also known as lesions, the UI team led by Reber and Aaron Boes, MD, PhD, correlated the level of connectedness of the damaged areas with the level of cognitive disability the patient experienced. The findings suggest that damage to highly connected regions of white matter is more predictive of cognitive impairment than damage to highly connected gray matter hubs.

Network hubs and brain function

Research on cognition often focuses on networks within the brain, and how different network configurations contribute to different aspects of cognition. Various mathematical models have been developed to measure the connectedness of networks and to identify hubs, or highly connected brain regions, that appear to be important in coordinating processing in brain networks.

The UI team used these well accepted mathematical models to identify the location of hubs within both gray and white matter from brain imaging of normal healthy individuals. The researchers then used brain scans from patients with brain lesions to find cases where areas of damage coincided with hubs. Using data from multiple cognitive tests for those patients, they were also able to measure the effect hub damage had on cognitive outcomes. Surprisingly, damage to highly connected gray matter hubs did not have a strong association with poor cognitive outcomes. In contrast, damage to dense white matter hubs was strongly linked to impaired cognition.

“The brain isn’t a blank canvas where all regions are equivalent; a small lesion in one region of the brain may have very minimal impact on cognition, whereas another one may have a huge impact. These findings might help us better predict, based on the location of the damage, which patients are at risk for cognitive impairment after stroke or other brain injury,” says Boes, UI professor of pediatrics, neurology, and psychiatry, and a member of the Iowa Neuroscience Institute. “It’s better to know those things in advance as it gives patients and family members a more realistic prognosis and helps target rehabilitation more effectively.”

UI registry is a unique resource for neuroscientists

Importantly, the new findings were based on data from over 500 individual patients, which is a large number compared to previous studies and suggests the findings are robust. The data came from two registries; one from Washington University in St. Louis, which provided data from 102 patients, and the Iowa Neurological Registry based at the UI, which provided data from 402 patients. The Iowa registry is over 40 years old and is one of the best characterized patient registries in the world, with close to 1000 subjects with well characterized cognition derived from hours of paper and pencil neuropsychological tests, and detailed brain imaging to map brain lesions. The registry is directed by Daniel Tranel, PhD, UI professor of neurology, and one of the study authors.

Reber notes that the study also illustrates the value of working with clinical patients as well as healthy individuals in terms of understanding relationships between brain structure and function.

“There is a lot of really excellent research using functional brain imaging with healthy participants or computer simulations that tell us that these gray matter hubs are critical to how the brain works, and that you can use them to predict how well healthy people will perform on cognitive tests. But when we look at how strokes and other brain damage actually affect people, it turns out that you can predict much more from damage to white matter,” he says. “Research with people who have survived strokes or other brain damage is messy, complicated, and absolutely essential, because it builds a bridge between basic scientific theory and clinical practice, and it can improve both.

I cannot stress enough how grateful we are that these patients have volunteered their time to help us; without them, a lot of important research would be impossible,” he adds.

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International study links brain thinning to psychosis — ScienceDaily


Subtle differences in the shape of the brain that are present in adolescence are associated with the development of psychosis, according to an international team led by neuroscientists at the University of Pittsburgh School of Medicine and Maastricht University in the Netherlands.

In results published today in JAMA Psychiatry, the differences are too subtle to detect in an individual or use for diagnostic purposes. But the findings could contribute to ongoing efforts to develop a cumulative risk score for psychosis that would allow for earlier detection and treatment, as well as targeted therapies. The discovery was made with the largest-ever pooling of brain scans in children and young adults determined by psychiatric assessment to be at high risk of developing psychosis.

“These results were, in a sense, sobering,” said Maria Jalbrzikowski, Ph.D., assistant professor of psychiatry at Pitt. “On the one hand, our data set includes 600% more high-risk youth who developed psychosis than any existing study, allowing us to see statistically significant results in brain structure. But the variance between whether or not a high-risk youth develops psychosis is so small that it would be impossible to see a difference at the individual level. More work is needed for our findings to be translated into clinical care.”

Psychosis is an umbrella term for a constellation of severe mental disorders that cause people to have difficulty determining what is real and what is not. Most often, individuals have hallucinations where they see or hear things that others do not. They also may have strongly held beliefs, or delusions, even when most people do not believe them. Schizophrenia is only one disorder associated with psychosis, and psychotic symptoms can occur in other psychiatric disorders, such as bipolar disorder, depression, body dysmorphic disorder or post-traumatic stress disorder. In people who receive a diagnosis of psychosis, there is a great deal of heterogeneity in outcomes over time.

Diagnosis usually happens in later adolescence and early adulthood, but most often symptoms begin to manifest in the teen years, when clinicians can use psychological assessments to determine a person’s risk of developing full-blown psychosis.

Jalbrzikowsi and Dennis Hernaus, Ph.D., assistant professor in the School of Mental Health and Neuroscience at Maastricht University, are co-chairs of the Enhancing Neuro Imaging Genetics Through Meta-Analysis (ENIGMA) Clinical High Risk for Psychosis Working Group. This group pooled structural magnetic resonance imaging (MRI) scans from 3,169 volunteer participants at an average age of 21 who were recruited at 31 different institutions. About half — 1,792 of the participants — had been determined to be at “clinical high risk for developing psychosis.” Of those high-risk participants, 253 went on to develop psychosis within two years. The co-chairs emphasized that this study would not be possible without the collaborative efforts of the 100-plus researchers involved.

When looking at all the scans together, the team found that those at high risk for psychosis had widespread lower cortical thickness, a measure of the thickness of the brain’s gray matter. In high-risk youth who later developed psychosis, a thinner cortex was most pronounced in several temporal and frontal regions.

Everyone goes through a cortical thinning process as they develop into an adult, but the team found that in younger participants between 12 and 16 years old who developed psychosis the thinning was already present. These high-risk youth who developed psychosis also progressed at a slower rate than in the control group.

“We don’t yet know exactly what this means, but adolescence is a critical time in a child’s life — it’s a time of opportunity to take risks and explore, but also a period of vulnerability,” Jalbrzikowski said. “We could be seeing the result of something that happened even earlier in brain development but only begins to influence behavior during this developmental stage.”

Hernaus stressed that these findings underscore the importance of early detection and intervention in people who show risk factors for developing psychosis, which include hearing whispers from voices that aren’t there and a family history of psychosis.

“Until now, researchers have primarily studied how the brains of people with clinical high risk for psychosis differ at a given point in time,” Hernaus said. “An important next step is to better understand brain changes over time, which could provide new clues on underlying mechanisms relevant to psychosis.”

This research received support from numerous funders listed in the JAMA Psychiatry manuscript. Jalbrzikowski received support from National Institute of Mental Health grant K01 MH112774.

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Sleep, stress, or hormones? Brain fog during perimenopause



Often when people think of perimenopause, irregular periods and hot flashes come to mind. But some women may notice another symptom: brain fog.

You’re reading a letter and suddenly realize your thoughts have drifted off and you need to start again. Or you draw a blank when you’re trying to remember someone’s name, or find yourself standing in a room, wondering what you came there to get.

The good news is that these small cognitive blips are probably not anything you need to worry about long-term.

Sleep disturbances and stress may be part of brain fog

Those times when you are less focused and a bit forgetful are likely not just due to hormonal changes. Sleep quality, perhaps related to night sweats during perimenopause, could definitely contribute. Increased stress that sometimes accompanies this stage of life may also have you feeling frazzled and distracted. These factors can interfere with concentration and memory.

Not getting enough sleep can leave you feeling cranky and sluggish. This may be why you can’t remember what’s-her-name: you weren’t paying close enough attention when she told you her name in the first place.

Stress can have a similar effect by pulling your thoughts off task, because you’re preoccupied, worrying about something else.

What can you do to feel less foggy?

If this sounds like you, there are some things you can do to help lift the fog and get your brain re-engaged.

  • Slow down. Train yourself to recognize when you’re distracted, and take a moment to breathe and refocus on the task at hand. If you’ve just taken in some new information, try to find a quiet moment to give your brain a chance to process what you’ve learned.
  • Manage your stress. Using mindful meditation or other stress-reduction strategies can also help you to relax and be more present. This can help you absorb new information and recall it more easily.
  • Get regular exercise. Physical activity benefits not only your body, but also your mind. One study found that just three days a week of moderate-intensity exercise appeared to increase the size of the hippocampus, a part of the brain involved in memory and learning.
  • Improve your sleep habits. If you are experiencing poor sleep quality, work on strategies that can help you get more rest at night. Improve your sleep hygiene by making changes, such as staying off electronic devices close to bedtime and establishing a regular sleep schedule. Check with your doctor if at-home strategies aren’t doing the trick.
  • Use memory tricks. Did you ever use little tricks to remember things when you were studying for a test in school? Those same mental cheats can help you now as well. For example, make up a mnemonic or a rhyme to help you recall information. Or try using visual or verbal clues. Repeating information or instructions to yourself or someone else is another way to help your brain store information more effectively.

Know when to seek help

Most small memory lapses are nothing to worry about. If changes due to perimenopause — including irregular periods, trouble sleeping due to night sweats, or brain fog — bother you, talk to your doctor about possible solutions.

It’s also important to call your doctor if

  • memory changes come on suddenly, or are accompanied by hallucinations, paranoia, or delusions
  • memory lapses might put your safety at risk, such as affecting your driving or forgetting food cooking on the stove.

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Key brain molecule may play role in many brain disorders — ScienceDaily


A team led by scientists at the UNC School of Medicine identified a molecule called microRNA-29 as a powerful controller of brain maturation in mammals. Deleting microRNA-29 in mice caused problems very similar to those seen in autism, epilepsy, and other neurodevelopmental conditions.

The results, published in Cell Reports, illuminate an important process in the normal maturation of the brain and point to the possibility that disrupting this process could contribute to multiple human brain diseases.

“We think abnormalities in microRNA-29 activity are likely to be a common theme in neurodevelopmental disorders and even in ordinary behavioral differences in individuals,” said senior author Mohanish Deshmukh, PhD, professor in the UNC Department of Cell Biology & Physiology and member of the UNC Neuroscience Center. “Our work suggests that boosting levels of miR-29, perhaps even by delivering it directly, could lead to a therapeutic strategy for neurodevelopmental disorders such as autism.”

miR-29 and brain maturation

MicroRNAs are short stretches of ribonucleic acid inside cells that regulate gene expression. Each microRNA, or miR, can bind directly to an RNA transcript from certain other genes, preventing it from being translated into a protein. MiRNAs thus effectively serve as inhibitors of gene activity, and the typical microRNA regulates multiple genes in this way so that genetic information is not overexpressed. These essential regulators have been intensively researched only in the past two decades. Therefore, much remains to be discovered about their roles in health and disease.

Deshmukh and colleagues set out to find microRNAs involved in the maturation of the brain after birth, a phase that in humans includes approximately the first 20 years of life. When the scientists looked for microRNAs with more activity in the adult mouse brain than the young mouse brain, one set of miRNA stuck way out from the rest. Levels of the miR-29 family were 50 to 70 times higher in the adult mouse brains than in young mouse brains.

The researchers examined a mouse model in which the genes for the miR-29 family were deleted just in the brain. They observed that although the mice were born normally, they soon developed a mix of problems, including repetitive behaviors, hyperactivity, and other abnormalities typically seen in mouse models of autism and other neurodevelopmental disorders. Many developed severe epileptic seizures.

To get a sense of what caused these abnormalities, the researchers examined gene activity in the brains of the mice, comparing it to activity in mouse brains that had miR-29. As expected, many genes were much more active when miR-29 was no longer there to block their activity. But the scientists unexpectedly found a large set of genes — associated with brain cells — that were less active in miR-29’s absence.

A mysterious methylator

With key assistance from co-author Michael Greenberg, PhD, a professor of neuroscience at Harvard University, the researchers eventually found the explanation for this mysterious reduction in gene activity.

One of the target genes that miR-29 normally blocks is a gene that encodes for an enzyme called DNMT3A. This enzyme places special chemical modifications called CH-methylations onto DNA, to silence genes in the vicinity. In mice brains, the activity of the gene for DNMT3A normally rises at birth and then sharply declines several weeks later. The scientists found that miR-29, which blocks DNMT3A, is what normally forces this sharp decline.

Thus, in the mice whose brains lack miR-29, DNMT3A is not suppressed and the CH-methylation process continues abnormally — and many brain cell genes that should become active continue to be suppressed instead. Some of these genes, and the gene for DNMT3A itself, have been found to be missing or mutated in individuals with neurodevelopmental disorders such as autism, epilepsy, and schizophrenia.

To confirm DNMT3A’s role, the scientists created a unique mouse model that prevents miR-29 from suppressing DNMT3A, but leaves miR-29’s other targets untouched. They showed that this unleashing of DNMT3A on its own results in many of the same problems such as seizures and early death, as seen in the mice without miR-29.

The findings highlight and clarify what seems likely to be a crucial process in shaping the brain late in its development: the switching-off of DNMT3A to free up many genes that are meant to be more active in the adult brain.

“These results are the first to identify miR-29 as an essential regulator of CH methylation, and to show why restricting CH methylation to a critical period is important for normal brain maturation,” Deshmukh said.

Deshmukh and colleagues are now following up by studying in more detail how the lack of miR-29 in different sets of brain cells might give rise to such disorders, and more generally they are studying how miR-29’s activity is regulated in childhood to fine-tune brain functions, thereby giving humans the traits that make them unique individuals.

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Look Ma, No Wires: Charging The Next Generation of Brain Implants



AsianScientist (Mar. 29, 2021) – In a mind-blowing development, researchers have engineered brain implants that can be wirelessly recharged outside the body—allowing extended control over neural circuits without battery replacement. Their findings were published in Nature Communications.

With their potential to read and even control minds, brain implants have long been a staple of science fiction. Far from being used for sinister means, brain implants actually impart real health benefits to patients with neurological conditions like epilepsy and Parkinson’s disease.

However, traditional tethered brain implants often cause stress and inflammation in freely-moving animals, reducing the device’s lifetime in the process. Though wireless versions have since been developed, such technologies still require occasional surgeries for battery replacement or bulky and inconvenient wireless power set-ups.

Upgrading the wireless brain implant he had developed in 2019, Professor Jeong Jae-Woong from the Korea Advanced Institute of Science and Technology (KAIST) developed a device composed of ultra-soft polymers that can be remotely controlled by a smartphone.

In the implant, LEDs the size of a grain of salt are mounted on probes as thick as a strand of human hair—allowing for the wireless control of target neurons in the deep brain using light. To make wireless battery charging and control possible, the team developed a tiny circuit that integrates a wireless energy harvester and a Bluetooth chip.

Magnetic waves penetrate brain tissue to generate electricity in the implant, charging it in the process. Meanwhile, the Bluetooth implant delivers programmable patterns of light to brain cells using a smartphone app, enabling real-time mind control.

To test the effectiveness of their technology, Jeong and his team implanted their device into cocaine-addled rats. By using the smartphone app to deliver precise bursts of light to relevant neurons in the rats’ brains, the researchers successfully suppressed the rodents’ cocaine-induced frenzy. As the rats moved about, the surrounding magnetic field ensured the repeated recharging of the implants’ batteries.

“This device can be operated anywhere and anytime to manipulate neural circuits, which makes it a highly versatile tool for investigating brain functions,” said lead author Mr. Kim Choong Yeon from KAIST.

Moving forward, the authors anticipate that the convenience offered by their wireless brain implant will lead to new therapeutic interventions for brain disorders and neurodegenerative diseases.

“This powerful device eliminates the need for additional painful surgeries to replace an exhausted battery in the implant, allowing seamless chronic neuromodulation,” said Jeong. “We believe that the same basic technology can be applied to various types of implants, including deep brain stimulators, and cardiac and gastric pacemakers, to reduce the burden on patients for long-term use within the body.”

The article can be found at: Kim et al. (2021) Soft Subdermal Implant Capable of Wireless Battery Charging and Programmable Controls for Applications in Optogenetics.

———

Source: Korea Advanced Institute of Science and Technology.
Disclaimer: This article does not necessarily reflect the views of AsianScientist or its staff.


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