Category: Neurology

Categories : Cardiovascular Disease NeurologyTags :

Vigorous Exercise Improves Walking in Chronic Stroke Patients

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When 67-year-old Larry Christian suffered a sudden loss of balance, he was diagnosed with a haemorrhagic stroke, and referred to the University of Delaware’s Physical Therapy Clinic for rehabilitation. 

“Initially, I had a lot of balance problems that we worked pretty intensely to correct,” Christian said. 

He enrolled in a clinical trial at UD, led by co-investigator Darcy Reisman, professor and chair of the Department of Physical Therapy, that sought to explore whether high-intensity interval training (HIIT) aids in improved gait post-stroke. UD was one of three sites selected for the clinical trial led by primary investigator and associate professor Pierce Boyne of the University of Cincinnati. Sandra Billinger, professor and vice chair of stroke translation research at the University of Kansas Medical Center, is also a co-investigator and represents the third site involved in the clinical trial. 

Now, seven years later, Christian is walking better. 

“Participating in this study got me to a point where I could walk better and even take a walk outside,” Christian said. “I’ve been pretty healthy all my life, and while I can’t play volleyball anymore, walking again made me feel great.”

Christian is among the lucky ones. Among 7 million stroke survivors in the US, fewer than 10% have adequate walking speed and endurance to complete normal daily activities like grocery shopping. 

Reisman said the results of the multi-million-dollar, five-year clinical trial showed HIIT helped more people than just Christian. The results, published in JAMA Neurology, show that chronic stroke survivors who engaged in high-intensity exercise with bursts of maximum-speed walking alternated with recovery periods saw a significant difference in their walking capacity over 12 weeks. The improvements were so dramatic Boyne and Reisman have secured a clinical trial grant renewal to triple the size of their study to 165 participants. 

She added HIIT looks different for each stroke survivor, and the optimal exercise program for each person with stroke remains unknown. 

“We want them to train at the fastest possible speed, which varies from person to person,” Reisman said. “But we don’t want them running.”

For those already walking at a reasonably fast pace, research associate Henry Wright in Reisman’s lab will add an incline or a weighted vest or wrap a bungee cord around their waist to create resistance. 

“It’s self-reported data, but participants tell me they have more energy, or they’re able to do more around the house, or they’re not winded when they go shopping,” Wright said. “By the end of the training, I can see their walking is smoother, they’re getting farther on clinical testing, and it’s rewarding to see their gains.”  

The results from the initial clinical trial showed Reisman and collaborators that HIIT was feasible and safe in a small group of stroke survivors, who saw sustained gains in walking capacity, more so than patients engaged in moderate-intensity exercise. 

However, further study of the intervention in larger populations is crucial to change the standard of care.

“Many physical therapists were trained during a time when patients with neurologic conditions, particularly stroke, were treated with kid gloves, partly because they say stroke is the heart attack of the brain,” Reisman said. “It’s common they also have cardiovascular conditions, so people tend to be extra careful with those patients in terms of pushing them.

“But what we know now is at least moderate-intensity, and likely high-intensity interval training, is essential not only for stroke survivors’ cardiovascular system but also for their brain,” Reisman said. “The evidence shows that intensity is linked to the release of neurotrophins in the brain that help the brain remodel after a stroke.” 

Kiersten McCartney, a physical therapist obtaining her doctorate in biomechanics and movement science, worked on the clinical trial with Reisman. She spent the 2022 Winter Session at Magee Rehabilitation Hospital in Philadelphia, helping them implement moderate-to-high-intensity exercise and saw the benefits first-hand. 

“I’ll never be able to say there’s no risk of heart attack. Even the fittest people can have a heart attack when exercising,” McCartney said. “Still, the data points to the idea that you’re doing more harm than good by not engaging your patients with stroke in high-intensity exercise when we talk about those longer-term outcomes.”

The HIIT-Stroke Trial 2 will continue to examine dosing to confirm whether a full 12 weeks of vigorous exercise is needed to see significant improvements in walking. Reisman and collaborators will identify whether differences in sex and other factors played a role in rehabilitation. If the five-year study results are similar and show significant gains from high-intensity interval exercise in a larger population, investigators would next work with NIH Strokenet to launch a nationwide clinical trial in people with stroke.  

“We’ve known about the value of moderate-intensity exercise for more than a decade, and it’s still not the standard of care,” Reisman said. “If we find that HIIT is the optimal intervention, the next phase would be the knowledge translation phase, where we’d systematically develop a methodology to get HIIT into clinics.” 

For HIIT to work as an intervention, Reisman said therapists will need the proper tools. She’s been pushing for commercially available heart rate monitors, placed around the chest during exercise, to be the standard of care in clinics for years.

“They’re already a standard of care for people in the community,” Reisman said. “Getting them into clinics is imperative so PTs can monitor patients’ heart rate the entire time they exercise. That constant monitoring gives therapists data on how a person is responding beyond visible signs and symptoms, and in turn, more peace of mind.” 

But beyond tools and training, Reisman said, it comes down to evidence and education. 

“If we have hundreds and hundreds of stroke survivors who’ve gone through our high-intensity exercise intervention, and we’ve seen no major adverse events – that will help,” Reisman said. “The more data we have to show therapists, the better we can implement this intervention that will change lives.”

Source: University of Delaware

Categories : NeurologyTags :

Poor Sleep Quality in Midlife Linked to Cognitive Problems Later on

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Photo by Andrea Piacquadio

People who have more disrupted sleep in their 30s and 40s may be more likely to have memory and thinking problems a decade later, according to new research published in Neurology. The study does not however prove that sleep quality causes cognitive decline, it only shows an association.

“Given that signs of Alzheimer’s disease start to accumulate in the brain several decades before symptoms begin, understanding the connection between sleep and cognition earlier in life is critical for understanding the role of sleep problems as a risk factor for the disease,” said study author Yue Leng, PhD, of the University of California, San Francisco.

“Our findings indicate that the quality rather than the quantity of sleep matters most for cognitive health in middle age.”

The study involved 526 people, average age of 40, who were followed for 11 years. Researchers looked at participants’ sleep duration and quality, and had them perform cognitive tests.

Participants wore a wrist activity monitor for three consecutive days on two occasions approximately one year apart to calculate their averages. Participants slept for an average of six hours.

Participants also reported bedtimes and wake times in a sleep diary and completed a sleep quality survey with scores ranging from zero to 21, with higher scores indicating poorer sleep quality. A total of 239 people, or 46%, reported poor sleep with a score greater than five. Participants also completed a series of memory and thinking tests.

Researchers also looked at sleep fragmentation, which measures repetitive short interruptions of sleep. They looked at both the percentage of time spent moving and the percentage of time spent not moving for one minute or less during sleep. Added together, participants had an average sleep fragmentation of 19%.

Researchers then divided participants into three groups based on their sleep fragmentation score. Of the 175 people with the most disrupted sleep, 44 had poor cognitive performance 10 years later, compared to 10 of the 176 people with the least disrupted sleep.

After adjusting for age, gender, race, and education, people who had the most disrupted sleep had more than twice the odds of having poor cognitive performance when compared to those with the least disrupted sleep.

There was no difference in cognitive performance at midlife for those in the middle group compared to the group with the least disrupted sleep.

“More research is needed to assess the link between sleep disturbances and cognition at different stages of life and to identify if critical life periods exist when sleep is more strongly associated with cognition,” Leng said.

“Future studies could open up new opportunities for the prevention of Alzheimer’s disease later in life.”

The amount of time people slept and their own reports of the quality of their sleep were not associated with cognition in middle age.

Source: American Academy of Neurology

Categories : Cancer NeurologyTags :

A New Way to Prevent Cognitive Decline from Radiotherapy

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Photo by National Cancer Institute on Unsplash

Microglia, the brain’s immune cells, can trigger cognitive deficits after radiation exposure and may be a key target for preventing these symptoms, University of Rochester researchers have found. Their work, published in the International Journal of Radiation Oncology Biology Biophysics, builds on previous research showing that after radiation exposure microglia damage synapses, the connections between neurons that are important for cognitive behaviour and memory.

“Cognitive deficits after radiation treatment are a major problem for cancer survivors,” M. Kerry O’Banion, MD, PhD, professor of Neuroscience, member of the Wilmot Cancer Institute, and senior author of the study said.

“This research gives us a possible target to develop therapies to prevent or mitigate against such deficits in people who need brain radiotherapy.”

Using several behavioural tests, researchers investigated the cognitive function of mice before and after radiation exposure.

Female mice performed the same throughout, indicating a resistance to radiation injury but Male mice could not remember or perform certain tasks after radiation exposure.

This cognitive decline correlates with the loss of synapses and evidence of potentially damaging microglial over-reactivity following the treatment.

Researchers then targeted the pathway in microglia important to synapse removal. Mice with these mutant microglia had no cognitive decline following radiation. And others that were given the drug, Leukadherin-1, which is known to block this same pathway, during radiation treatment, also had no cognitive decline.

“This could be the first step in substantially improving a patient’s quality of life and need for greater care,” said O’Banion. “Moving forward, we are particularly interested in understanding the signals that target synapses for removal and the fundamental signaling mechanisms that drive microglia to remove these synapses. We believe that both avenues of research offer additional targets for developing therapies to help individuals receiving brain radiotherapy.”

O’Banion also believes this work may have broader implications because some of these mechanisms are connected to Alzheimer’s and other neurodegenerative diseases.

Source: University of Rochester Medical Center

Categories : Lab Tests and Imaging Neurology UncategorizedTags :

Macrophages Light up Mild Brain Injuries for MRI

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Coup and contrecoup brain injury. Credit: Scientific Animations CC4.0

Researchers have created a new brain imaging method that allows to be diagnosed, even when existing imaging techniques like magnetic resonance imaging (MRI) The technique involves loading gadolinium, a standard MRI contrast agent, into ‘backpacks’ that are attached macrophages. mTBIs cause inflammation, attracting macrophages there. Coupling the gadolinium contrast agent to these cells enables MRI to reveal brain inflammation and increase the number of correctly diagnosed mTBI cases, improving patient care. The method is described in a new paper in Science Translational Medicine.

“70-90% of reported TBI cases are categorised as ‘mild,’ yet as many as 90% of mTBI cases go undiagnosed, even though their effects can last for years and they are known to increase the risk of a host of neurological disorders including depression, dementia, and Parkinson’s disease,” said senior author Samir Mitragotri, PhD, in whose lab the research was performed. “Our cell-based imaging approach exploits immune cells’ innate ability to travel into the brain in response to inflammation, enabling us to identify mTBIs that standard MRI imaging would miss.”

Using immune cells to identify inflammation

Most of us know someone who has had a concussion (another name for an mTBI), sometimes even more than one. But the vast majority of people who experience an mTBI are never properly diagnosed. Without that diagnosis, they can exacerbate their injuries by returning to normal activity before they’re fully recovered, which can lead to further damage. Some studies even suggest that repeated mTBIs can lead to chronic traumatic encephalopathy (CTE), the neurodegenerative disease that has been found to afflict more than 90% of professional American football players.

Because the effects of mTBI are believed to be caused by “invisible” brain inflammation, members of the Mitragotri lab decided to leverage their experience with immune cells to create a better diagnostic. “Our previous projects have focused on controlling the behaviour of immune cells or using them to deliver drugs to a specific tissue. We wanted to exploit another innate ability of immune cells – homing to sites of inflammation in the body – to carry imaging agents into the brain, where they can provide a visible detection signal for mTBI,” said first author Lily Li-Wen Wang, Ph.D.. Wang is a former Research Fellow in the Mitragotri Lab at the Wyss Institute and SEAS who is now a scientist at Landmark Bio.

Gadolinium needs water to show up on MRI

The team planned to use their cellular backpack technology to attach gadolinium molecules to macrophages, known to infiltrate the brain in response to inflammation. But right away, they ran into a problem: in order to function as a contrast agent for MRI scans, gadolinium needs to interact with water. Their original backpack microparticles are made of a hydrophobic polymer called PLGA. So Wang and her co-authors started developing a new backpack made out of a hydrogel material that could be manufactured at a large scale in the lab.

After years of hard work, they finally created a new hydrogel backpack that could produce a strong gadolinium-mediated MRI signal, attach stably to both mouse and pig macrophages, and maintain their cargo for a sustained period of time in vitro. They named their new microparticles M-GLAMs, short for “macrophage-hitchhiking Gd(III)-Loaded Anisotropic Micropatches.” Now, it was time to test them in a more realistic setting, for which they partnered with researchers and clinicians at Boston Children’s Hospital.

First, they injected mouse M-GLAMs macrophages into mice to see if they could visualize them in vivo. They were especially interested to see if they accumulated in the kidney, as existing gadolinium-based contrast agents like Gadavist® can cause health risks for patients with kidney disease. Their M-GLAMs did not accumulate in the mice’s kidneys, but persisted in their bodies for over 24 hours with no negative side effects. In contrast, mice injected with Gadavist® showed substantial accumulation of the contrast agent in their kidneys within 15 minutes of injection, and the substance was fully cleared from their bodies within 24 hours.

Then, they tested porcine M-GLAMs in a pig model of mTBI. They injected the M-GLAMs into the animals’ blood two days after a mock mTBI, then used MRI to evaluate the concentration of gadolinium in the brain. They focused on a small region called the choroid plexus, which is known as a major conduit of immune cells into the brain. Pigs that received the M-GLAMs displayed a significant increase in the intensity of gadolinium present in the choroid plexus, while those injected with Gadavist® did not, despite confirmation of increased inflammation macrophage density in the brains of both groups. The animals showed no toxicity in any of their major organs following administration of the treatments.

“Another important aspect of our M-GLAMs is that we are able to achieve better imaging at a much lower dose of gadolinium than current contrast agents – 500-1000-fold lower in the case of Gadavist®,” said Wang. “This could allow the use of MRI for patients who are currently unable to tolerate existing contrast agents, including those who have existing kidney problems.”

Source: Wyss Institute for Biologically Inspired Engineering at Harvard

Categories : Ageing NeurologyTags :

Older Adults’ Migraine Diagnosis Linked to Tripled Risk of Vehicle Crash

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A new study from researchers at the University of Colorado Anschutz Medical Campus finds that older adult drivers who are recently diagnosed with migraines are three times as likely to experience a motor vehicle crash. Older adult drivers who reported having ever had migraines in the past were no more likely to have a motor vehicle crash than those without migraines.

The study, published in the Journal of the American Geriatrics Society, also explored the relationships medications commonly prescribed for migraine management have with increased crash risk.

“Migraine headaches affect more than 7% of US adults over the age of 60,” says Carolyn DiGuiseppi, MPH, PhD, MD, professor with the Colorado School of Public Health and study lead author.

“The US population is aging, which means increasing numbers of older adult drivers could see their driving abilities affected by migraine symptoms previously not experienced. These symptoms include sleepiness, decreased concentration, dizziness, debilitating head pain and more.”

Researchers conducted a five-year longitudinal study of more than 2500 active drivers aged 65-79 in five sites across the United States.

Participants were categorised as having previously been diagnosed with migraine symptoms (12.5%), no previous diagnosis but experienced symptoms during the study timeframe (1.3%) or never migraine respondents.

Results indicate those with previous diagnosis did not have a different likelihood of having crashes after baseline, while those with new onset migraines were three times as likely to experience a crash within one year of diagnosis.

Previously diagnosed drivers nevertheless had experienced more hard braking events compared to adults who had never experienced a migraine.

Additionally, researchers examined the role medications commonly prescribed for migraines have in motor vehicle events and found that there was no impact on the relationship between migraines and either crashes or driving habits.

Few participants in the study sample were using acute migraine medications, however.

“These results have potential implications for the safety of older patients that should be addressed,” says DiGuiseppi. “Patients with a new migraine diagnosis would benefit from talking with their clinicians about driving safety, including being extra careful about other risks, such as distracted driving, alcohol, pain medication and other factors that affect driving.”

Source: University of Colorado Anschutz Medical Campus

Categories : Neurodegenerative Diseases NeurologyTags :

Could Stimulating Gamma Brain Waves Help Treat Alzheimer’s?

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Photo by JD Mason on Unsplash

A review in the Journal of Internal Medicine explores the potential of non-invasive interventions such as light, sound, and magnets to stimulate gamma brain waves for the treatment of Alzheimer’s disease. Such strategies may be beneficial because Alzheimer’s disease is characterised by reduced fast brain oscillations in the gamma range (30–100Hz).

The authors note that recent studies reveal that it is feasible and safe to induce 40Hz brain activity in patients with Alzheimer’s disease through a range of methods. Also, preliminary evidence suggests that such treatment can yield beneficial effects on brain function, disease pathology, and cognitive function in patients.

Various cells in the brain beyond neurons, including microglial cells, astrocytes and vascular cells, seem to be involved in mediating these effects.

“We found that increased gamma activity elicited by the non-invasive 40Hz sensory stimulation profoundly alters the cellular state of various glial cell types,” said corresponding author Li-Huei Tsai, PhD, of MIT. “We are actively investigating the mechanism by which the 40Hz brain activity recruits diverse cell types in the brain to provide neuroprotective effects.”

Source: Wiley

Categories : Neurology Respiratory DiseasesTags :

How Measles Spreads to the Brain in Rare Cases

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Mayo Clinic researchers mapped how the measles virus mutated and spread in the brain of a person who succumbed to a rare, lethal brain disease. New cases of this disease, which is a complication of the measles virus, may occur as measles re-emerges among the unvaccinated, say researchers.

Using the latest tools in genetic sequencing, researchers at Mayo Clinic reconstructed how a collective of viral genomes colonised a human brain.

The virus acquired distinct mutations that drove the spread of the virus from the frontal cortex outward.

The highly contagious measles virus infects the upper respiratory tract where it uses the trachea as a trampoline to launch and spread through droplets dispersed when an infected person coughs or sneezes.

Dr Cattaneo pioneered studies on how the measles virus spreads throughout the body. He first began to study the measles virus about 40 years ago and was fascinated by the rare, lethal brain disease called subacute sclerosing panencephalitis (SSPE), which occurs in about 1 in every 10 000 measles cases.

It can take about five to 10 years after the initial infection for the measles virus to mutate and spread throughout the brain.

Symptoms of this progressive neurological disease include memory loss, seizures and immobility.

Dr. Cattaneo studied SSPE for several years until the lethal disease nearly disappeared as more people were vaccinated against measles. But now, measles is resurging due to vaccine hesitancy and missed vaccinations.

During the COVID pandemic, millions of children missed receiving their measles vaccinations, which has resulted in an estimated 18% increase in measles cases and 43% increase in death from measles in 2021 compared to 2022 worldwide, according to a recent Centers for Disease Control and Prevention (CDC) report.

“We suspect SSPE cases will rise again as well. This is sad because this horrible disease can be prevented by vaccination. But now we are in the position to study SSPE with modern, genetic sequencing technology and learn more about it,” says Iris Yousaf, co-lead author of the study and a fifth-year Ph.D. candidate at Mayo Clinic Graduate School of Biomedical Sciences.

Dr Cattaneo and Yousaf had a unique research opportunity through a collaboration with the CDC. They studied the brain of a person who had contracted measles as a child and had succumbed to SSPE years later as an adult.

They investigated 15 specimens from different regions of the brain and conducted genetic sequencing on each region to piece together the puzzle of how the measles virus mutated and spread.

The researchers discovered that, after the measles virus entered the brain, its genome began to mutate in harmful ways over successive generations, creating a population of varied genomes.

“In this population, two specific genomes had a combination of characteristics that worked together to promote virus spread from the initial location of the infection – the frontal cortex of the brain – out to colonise the entire organ,” says Dr Cattaneo.

The next steps in this research are to understand how specific mutations favour virus spread in the brain. These studies will be done in cultivated brain cells brain organoids. This knowledge may help in creating effective antiviral drugs to combat virus spread in the brain. However, pharmacological intervention in advanced disease stages is challenging, and preventing SSPE through measles vaccination remains the best method.

Source: Mayo Clinic

Categories : Cancer NeurologyTags :

Little-studied Cell in the Brain could be Driver of Glioblastoma

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Photo by National Cancer Institute on Unsplash

Glioblastoma is one of the most treatment-resistant cancers, with those diagnosed surviving for less than two years. In a new study in NPJ Genomic Medicine, researchers at the University of Notre Dame have found that a largely understudied cell could offer new insight into how the aggressive, primary brain cancer is able to resist immunotherapy.

“A decade ago, we didn’t even know perivascular fibroblasts existed within the brain, and not just in the lining of the skull,” said senior author Meenal Datta, assistant professor of aerospace and mechanical engineering at Notre Dame.

“My lab’s expertise is examining tumours from an engineering and systems-based approach and looking at the novel mechanical features in rare cancers that may have been understudied or overlooked.”

Using standard bioinformatics and newer AI-based approaches, Datta’s TIME Lab began analysing different genes expressed in the tumour microenvironment related to the extracellular matrix – or the scaffolding cells create to support future cell adhesion, migration, proliferation and differentiation – and other various cell types.

What they found was a surprising, fairly new cell type: perivascular fibroblasts.

These fibroblasts are typically found in the blood vessels of a healthy brain and deposit collagen to maintain the structural integrity and functionality of brain vessels.

“It was a serendipitous discovery,” said first author Maksym Zarodniuk, graduate student in the TIME Lab and the bioengineering doctorate programme.

“We started in a completely different direction and stumbled upon this population of cells by using a combination of both bulk and single-cell RNA sequencing analyses of patient tumours.”

In their data, researchers were able to identify two groups of patients: those with a higher proportion of perivascular fibroblasts and those with significantly less.

They found that brain cancer patients with more perivascular fibroblasts in their tumours were more likely to respond poorly to immunotherapies and have poor survival outcomes.

Further study revealed that perivascular fibroblasts support the creation of an immunosuppressive tumour microenvironment, allowing the cancer to better evade the immune system.

The fibroblasts may also help the cancer resist therapies such as chemotherapy that targets cell division by promoting stem-like cancer cells that rarely divide, which are believed to be a major source of tumour relapse and metastasis.

“Moving forward, we want to do new experiments to confirm what we found in this paper and provide some good ground to start thinking about how to improve response to immunotherapy,” Zarodniuk said.

Because perivascular fibroblasts are a part of a healthy brain’s vasculature, Datta believes that these cells are breaking off and getting close to or infiltrating the glioblastoma tumour.

However, instead of supporting healthy brain function, these fibroblasts are getting reprogrammed and helping the tumour instead.

“Most people think about the brain as being very soft, with soft cells and a soft matrix. But by putting down these fibroblasts and making these very fibrous proteins, it gives us an entirely different perspective on the structure of the brain and how it can be taken advantage of by cancer cells originating in the same organ,” Datta said.

Source: University of Notre Dame

Categories : Injury & Trauma NeurologyTags :

Key Protein Coordinates Healing in Brain Injuries

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Image of an astrocyte, a subtype of glial cells. Glial cells are the most common cell in the brain. Credit: Pasca Lab, Stanford University NIH support from: NINDS, NIMH, NIGMS, NCATS

A new study published in PNAS Nexus provides a better understanding of how the brain responds to injuries. Researchers at the George Washington University discovered that a protein called Snail plays a key role in coordinating the response of brain cells after an injury.

The study shows that after an injury to the central nervous system (CNS), a group of localised cells start to produce Snail, a transcription factor or protein that has been implicated in the repair process. The GW researchers show that changing how much Snail is produced can significantly affect whether the injury starts to heal efficiently or whether there is additional damage.

“Our findings reveal the intricate ways the brain responds to injuries,” said senior author Robert Miller, the Vivian Gill Distinguished Research Professor and Vice Dean of the GW School of Medicine and Health Sciences.

“Snail appears to be a key player in coordinating these responses, opening up promising possibilities for treatments that can minimise damage and enhance recovery from neurological injuries.”

This study identified for the first time a special group of microglial-like cells that produce Snail. Microglial cells are found in the central nervous system. The researchers found that lowering the amount of Snail produced after an injury results in inflammation and increased cell death. During this process, the injury worsens and there are fewer connections or synapses between brain cells. In contrast, when Snail levels are increased the outcome of brain injury improves-suggesting this protein can help limit the spread of injury-induced damage.

The research raises questions about whether an experimental drug that affects Snail production could be used to limit the damage incurred after someone suffers a stroke or has been injured in an accident, Miller said.

Additional studies must be done to show that increasing Snail production could curtail injury or even promote healing of the brain.

Miller and his team also plan to study the regulation of Snail in diseases like multiple sclerosis, a disease resulting in damage to the myelin nerve sheath. If drugs targeting Snail could be used to stop that damage, many of the future symptoms of this disease could be eased, he says.

But researchers have years of work to do before new drugs targeting Snail can be tested in clinical trials. The payoff ultimately might be drugs that can lead to accelerated healing for stroke damage, head wounds and even neurodegenerative diseases like dementia.

Source: George Washington University

Categories : NeurologyTags :

What Happens When the Brain Loses a Hub?

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Photo by Jafar Ahmed on Unsplash

A University of Iowa-led team of international neuroscientists have obtained the first direct recordings of the human brain in the minutes before and after a brain hub crucial for language meaning was surgically disconnected. The results reveal the importance of brain hubs in neural networks and the remarkable way in which the human brain attempts to compensate when a hub is lost, with immediacy not previously observed. The findings were reported recently in the journal Nature Communications.

Hubs are critical for connectivity

The human brain has hubs – the intersection of many neuronal pathways that help coordinate brain activity required for complex functions like understanding and responding to speech. But debate has reigned as to whether highly interconnected brain hubs are irreplaceable for certain brain functions. By some accounts the brain, as an already highly interconnected neural network, can in principle immediately compensate for the loss of a hub, in the same way that traffic can be redirected around a blocked-off city centre.

With a rare experimental opportunity, the UI neurosurgical and research teams led by Matthew Howard III, MD, professor and DEO of neurosurgery, and Christopher Petkov, PhD, professor and vice chair for research in neurosurgery, have achieved a breakthrough in understanding the necessity of a single hub. By obtaining evidence for what happens when a hub required for language meaning is lost, the researchers showed both the intrinsic importance of the hub as well as the remarkable and rapid ability of the brain to adapt and at least partially attempt to immediately compensate for its loss.

Evaluating the impact of losing a brain hub

The study was conducted during surgical treatment of two patients with epilepsy. Both patients were undergoing procedures that required surgical removal of the anterior temporal lobe – a brain hub for language meaning – to allow the neurosurgeons access to a deeper brain area causing the patients’ debilitating epileptic seizures. Before this type of surgery, neurosurgery teams often ask the patients to conduct speech and language tasks in the operating room as the team uses implanted electrodes to record activity from parts of the brain close to and distant from the planned surgery area. These recordings help the clinical team effectively treat the seizures while limiting the impact of the surgery on the patient’s speech and language abilities.

Typically, the recording electrodes are not needed after the surgical resection procedure and are removed. The innovation in this study was that the neurosurgery team was able to safely complete the procedure with the recording electrodes left in place or replaced to the same location after the procedure. This made it possible to obtain rare pre- and post-operative recordings allowing the researchers to evaluate signals from brain areas far away from the hub, including speech and language areas distant from the surgery site. Analysis of the change in responses to speech sounds before and after the loss of the hub revealed a rapid disruption of signaling and subsequent partial compensation of the broader brain network.

“The rapid impact on the speech and language processing regions well removed from the surgical treatment site was surprising, but what was even more surprising was how the brain was working to compensate, albeit incompletely within this short timeframe,” says Petkov, who also holds an appointment at Newcastle University Medical School in the UK.

The findings disprove theories challenging the necessity of specific brain hubs by showing that the hub was important to maintain normal brain processing in language.

“Neurosurgical treatment and new technologies continue to improve the treatment options provided to patients,” says Howard, who also is a member of the Iowa Neuroscience Institute.

“Research such as this underscores the importance of safely obtaining and comparing electrical recordings pre and post operatively, particularly when a brain hub might be affected.”

According to the researchers, the observation on the nature of the immediate impact on a neural network and its rapid attempt to compensate provides evidence in support of a brain theory proposed by Professor Karl Friston at University College London, which posits that any self-organising system at equilibrium works towards orderliness by minimising its free energy, a resistance of the universal tendency towards disorder.

These neurobiological results following human brain hub disconnection were consistent with several predictions of this and related neurobiological theories, showing how the brain works to try to regain order after the loss of one of its hubs.

Source: University of Iowa Health Care