Tag: epilepsy

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An Arthritis Drug Might Unlock Lasting Relief from Epilepsy and Seizures

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A drug typically prescribed for arthritis halts brain-damaging seizures in mice that have a condition like epilepsy, according to researchers at the University of Wisconsin–Madison. The drug, called tofacitinib, also restores short-term and working memory lost to epilepsy in the mice and reduces inflammation in the brain caused by the disease.

If the drug proves viable for human patients, it would be the first to provide lasting relief from seizures even after they stopped taking it.

“It ticks all the boxes of everything we’ve been looking for,” says Avtar Roopra, a neuroscience professor in the UW–Madison School of Medicine and Public Health and senior author of the study, which appears in Science Translational Medicine.

Epilepsy is one of the most common neurological diseases, afflicting more than 50 million people around the world. While there are many known causes, the disease often appears after an injury to the brain, like a physical impact or a stroke.

Some days, months or even years after the injury, the brain loses the ability to calm its own activity. Normally balanced electrical activity through the brain goes haywire.

“The system revs up until all the neurons are firing all the time, synchronously,” says Roopra. “That’s a seizure that can cause massive cell death.”

And the seizures repeat, often at random intervals, forever. Some drugs have been useful in addressing seizure symptoms, protecting patients from some of the rampant inflammation and memory loss, but one-third of epilepsy patients do not respond to any known drugs, according to Olivia Hoffman, lead author of the study and a postdoctoral researcher in Roopra’s lab. The only way to stop the most damaging seizures has been to remove a piece of the brain where disruptive activity starts.

On their way to identifying tofacitinib’s potential in epilepsy, Hoffman and co-authors used relatively new data science methods to sift through the way thousands of genes were expressed in millions of cells in the brains of mice with and without epilepsy. They found a protein called STAT3, key to a cell signaling pathway called JAK, at the centre of activity in the seizure-affected mouse brains.

“When we did a similar analysis of data from brain tissue removed from humans with epilepsy, we found that was also driven by STAT3,” Hoffman says.

Meanwhile, Hoffman had unearthed a study of tens of thousands of arthritis patients in Taiwan aimed at describing other diseases associated with arthritis. It turns out, epilepsy was much more common among those arthritis patients than people without arthritis — but surprisingly less common than normal for the arthritis patients who had been taking anti-inflammatory drugs for more than five-and-a-half years.

“If you’ve had rheumatoid arthritis for that long, your doctor has probably put you on what’s called a JAK-inhibitor, a drug that’s targeting this signaling pathway we’re thinking is really important in epilepsy,” Hoffman says.

The UW researchers ran a trial with their mice, dosing them with the JAK-inhibitor tofacitinib following the administration of a brain-damaging drug that puts them on the road to repeated seizures. Nothing happened. The mice still developed epilepsy like human patients.

Remember, though, that epilepsy doesn’t often present right after a brain-damaging event. It can take years. In the lab mice, there’s usually a lull of weeks of relatively normal time between the brain damage and what the researchers call “reignition” of seizures. If it’s not really epilepsy until reignition, what if they tried the drug then? They devised a 10-day course of tofacitinib to start when the mouse brains fell out of their lull and back into the chaos of seizures.

“Honestly, I didn’t think it was going to work,” Hoffman says. “But we believe that initial event sort of primes this pathway in the brain for trouble. And when we stepped in at that reignition point, the animals responded.”

The drug worked better than they could have imagined. After treatment, the mice stayed seizure-free for two months, according to the paper. Collaborators at Tufts University and Emory University tried the drug with their own mouse models of slightly different versions of epilepsy and got the same, seizure-free results.

Roopra’s lab has since followed mice that were seizure-free for four and five months. And their working memory returned.

“These animals are having many seizures a day. They cannot navigate mazes. Behaviourally, they are bereft. They can’t behave like normal mice, just like humans who have chronic epilepsy have deficits in learning and memory and problems with everyday tasks,” Roopra says. “We gave them that drug, and the seizures disappear. But their cognition also comes back online, which is astounding. The drug appears to be working on multiple brain systems simultaneously to bring everything under control, as compared to other drugs, which only try to force one component back into control.”

Because tofacitinib is already FDA-approved as safe for human use for arthritis, the path from animal studies to human trials may be shorter than it would be for a brand-new drug. The next steps toward human patients largely await NIH review of new studies, which have been paused indefinitely amid changes at the agency.

For now, the researchers are focused on trying to identify which types of brain cells are shifted back to healthy behavior by tofacitinib and on animal studies of even more of the many types of epilepsy. Hoffman and Roopra have also filed for a patent on the use of the drug in epilepsy.

Source: University of Wisconsin-Madison

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New Cannabis Formula will Help Epilepsy, Multiple Sclerosis Sufferers

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Scientists at the University of South Australia have come up with an innovative solution to improve the effectiveness of cannabidiol to treat epilepsy, multiple sclerosis and other neurodegenerative diseases.

Cannabidiol (CBD), a non-psychoactive cannabis compound, is widely prescribed for its analgesic, anti-inflammatory and neuroprotective properties, but its clinical applications to date have been limited by its poor water solubility and absorption in the human body.

By developing a phospholipid complex – a class of lipids (fats) that contain phosphorus – UniSA researchers have increased the solubility of cannabidiol by up to six times and improved its absorption in the gastrointestinal tract.

Lead researcher Professor Sanjay Garg says the breakthrough, reported in the International Journal of Molecular Sciences, means that patients could experience more consistent and effective results with lower doses of oral CBD medications.

Currently, only a small fraction of orally ingested CBD reaches the bloodstream, limiting its therapeutic effects.

“For this reason, a number of different formulations have been explored, including the production of synthetic CBD, self-emulsifying delivery systems, and encapsulating CBD in gelatine matrix pellets, but all of them have only resulted in minor improvements in bioavailability,” Prof Garg says.

His research team identified the optimal phospholipid composition to form nanosized CBD-PLC particles. Compared to pure CBD, the phospholipid complex improved dissolution rates from 0% to 67.1% within three hours, demonstrating a significant enhancement in drug release.

In cellular uptake studies, CBD-PLC exhibited 32.7% higher permeability than unmodified CBD, ensuring greater absorption through the intestinal wall.

Another critical advantage of this new delivery system is its stability. Traditional CBD formulations degrade over time when exposed to heat, light or oxygen, reducing potency and shelf life.

However, testing over 12 months showed that CBD-PLC retained its performance under varied storage conditions, making it a more reliable option for pharmaceutical applications.

The study’s first author, UniSA PhD candidate Thabata Muta, says the discovery has significant implications for the future of CBD-based therapeutics.

“Improved bioavailability means that lower doses can achieve the same therapeutic effect, potentially reducing side effects and making treatment more cost effective,” Thabata says.

The research team believes that this innovation could be applied beyond CBD, providing a blueprint for enhancing the absorption of other poorly water-soluble drugs.

With the global CBD market projected to grow from USD 7.59 billion in 2023 to USD 202.45 billion by 2032, the findings of this study come at a crucial time, according to the study authors.

The team is now exploring opportunities for commercialisation and clinical trials to validate their new formulation.

Source: University of South Australia

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Do Seizures in Newborns Increase Children’s Risk of Developing Epilepsy?

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Seizures in newborns are one of the most frequent acute neurological conditions among infants admitted to neonatal care units. A study published in Developmental Medicine & Child Neurology indicates that newborns experiencing such neonatal seizures face an elevated risk of developing epilepsy.

For the study, investigators analysed data on all children born in Denmark between 1997 and 2018, with the goal of comparing the risk of epilepsy in children with and without neonatal seizures.

Among 1,294,377 children, the researchers identified 1,998 who experienced neonatal seizures. The cumulative risk of epilepsy was 20.4% among children with neonatal seizures compared with 1.15% among children without. This indicates that 1 in 5 newborns with neonatal seizures will develop epilepsy.

Epilepsy was diagnosed before 1 year of age in 11.4% of children with neonatal seizures, in an additional 4.5% between 1 and 5 years, 3.1% between 5 and 10 years, and 1.4% between 10 and 22 years. Stroke, hemorrhage, or structural brain malformations in newborns, as well as low Apgar scores, were associated with the highest risks of developing epilepsy.

“Our study highlights that there are risk factors that may be used to identify infants for tailored follow-up and preventive measures,” said corresponding author Jeanette Tinggaard, MD, PhD, of Copenhagen University Hospital – Rigshospitalet. “Importantly, four out of five neonatal survivors with a history of neonatal seizures did not develop epilepsy, and we suggest future studies to explore a potential genetic predisposition.”

Source: Wiley

Categories : Lab Tests and Imaging NeurologyTags :

New Tech could Cut Epilepsy Misdiagnoses by up to 70% Using Routine EEGs

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Doctors could soon reduce epilepsy misdiagnoses by up to 70% using a new tool that turns routine electroencephalogram, or EEG, tests that appear normal into highly accurate epilepsy predictors, a Johns Hopkins University study has found.

By uncovering hidden epilepsy signatures in seemingly normal EEGs, the tool could significantly reduce false positives, seen in around 30% of cases globally, and spare patients from medication side effects, driving restrictions, and other quality-of-life challenges linked to misdiagnoses.

“Even when EEGs appear completely normal, our tool provides insights that make them actionable,” said Sridevi V. Sarma, a Johns Hopkins biomedical engineering professor who led the work. “We can get to the right diagnosis three times faster because patients often need multiple EEGs before abnormalities are detected, even if they have epilepsy. Accurate early diagnosis means a quicker path to effective treatment.”

A report of the study is newly published in Annals of Neurology.

Epilepsy causes recurrent, unprovoked seizures triggered by bursts of abnormal electrical activity in the brain. Standard care involves scalp EEG recordings during initial evaluations. These tests track brainwave patterns using small electrodes placed on the scalp.

Clinicians partly rely on EEGs to diagnose epilepsy and decide whether patients need anti-seizure medications. However, EEGs can be challenging to interpret because they capture noisy signals and because seizures rarely occur during the typical 20 to 40 minutes of an EEG recording. These characteristics makes diagnosing epilepsy subjective and prone to error, even for specialists, Sarma explained.

To improve reliability, Sarma’s team studied what happens in the brains of patients when they are not experiencing seizures. Their tool, called EpiScalp, uses algorithms trained on dynamic network models to map brainwave patterns and identify hidden signs of epilepsy from a single routine EEG.

“If you have epilepsy, why don’t you have seizures all the time? We hypothesized that some brain regions act as natural inhibitors, suppressing seizures. It’s like the brain’s immune response to the disease,” Sarma said.

The new study analyzed 198 epilepsy patients from five major medical centers: Johns Hopkins Hospital, Johns Hopkins Bayview Medical Center, University of Pittsburgh Medical Center, University of Maryland Medical Center, and Thomas Jefferson University Hospital. Out of these 198 patients in the study, 91 patients had epilepsy while the rest had non-epileptic conditions mimicking epilepsy.

When Sarma’s team reanalysed the initial EEGs using EpiScalp, the tool ruled out 96% of those false positives, cutting potential misdiagnoses among these cases from 54% to 17%.

“This is where our tool makes a difference because it can help us uncover markers of epilepsy in EEGs that appear uninformative, reducing the risk of patients being misdiagnosed and treated for a condition they don’t have,” said Khalil Husari, co-senior author and assistant professor of neurology at Johns Hopkins. “These patients experienced side effects of the anti-seizure medication without any benefit because they didn’t have epilepsy. Without the correct diagnosis, we can’t find out what’s actually causing their symptoms.”

In certain cases, misdiagnosis happens due to misinterpretation of EEGs, Husari explained, as doctors may overdiagnose epilepsy to prevent the dangers of a second seizure. But in some cases, patients experience nonepileptic seizures, which mimic epilepsy. These conditions can often be treated with therapies that do not involve epilepsy medication.

In earlier work, the team studied epileptic brain networks using intracranial EEGs to demonstrate that the seizure onset zone is being inhibited by neighboring regions in the brain when patients are not seizing. EpiScalp builds on this research, identifying these patterns from routine scalp EEGs.

Traditional approaches to improve EEG interpretation often focus on individual signals or electrodes. Instead, EpiScalp analyses how different regions of the brain interact and influence one another through a complex network of neural pathways, said Patrick Myers, first author and doctoral student in biomedical engineering at Johns Hopkins.

“If you just look at how nodes are interacting with each other within the brain network, you can find this pattern of independent nodes trying to cause a lot of activity and the suppression from nodes in a second region, and they’re not interacting with the rest of the brain,” Myers said. “We check whether we can see this pattern anywhere. Do we see a region in your EEG that has been decoupled from the rest of the brain’s network? A healthy person shouldn’t have that.”

Source: Johns Hopkins University

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An Ancient Brain Area Processes Numerical Concepts

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Photo by Anna Shvets

New research in patients undergoing neurosurgery reveals the unique human ability to conceptualise numbers may be rooted deep within the brain. In good news for those who are stumped by maths, the results of the study by Oregon Health & Science University involving neurosurgery patients suggests new possibilities for tapping into those areas to improve learning.

“This work lays the foundation to deeper understanding of number, math and symbol cognition – something that is uniquely human,” said senior author Ahmed Raslan, MD, professor and chair of neurological surgery in the OHSU School of Medicine. “The implications are far-reaching.”

The study appears in the journal PLOS ONE.

Raslan and co-authors recruited 13 people with epilepsy who were undergoing a commonly used surgical intervention to map the exact location within their brains where seizures originate, a procedure known as stereotactic electroencephalography. During the procedure, researchers asked the patients a series of questions that prompted them to think about numbers as symbols (for example, 3), as words (“three”) and as concepts (a series of three dots).

As the patients responded, researchers found activity in a surprising place: the putamen.

Located deep within the basal ganglia above the brain stem, the putamen is an area of the brain primarily associated with elemental functions, such as movement, and some cognitive function, but rarely with higher-order aspects of human intelligence like solving calculus. Neuroscientists typically ascribe consciousness and abstract thought to the cerebral cortex, which evolved later in human evolution and wraps around the brain’s outer layer in folded grey matter.

“That likely means the human ability to process numbers is something that we acquired early during evolution,” Raslan said. “There is something deeper in the brain that gives us this capacity to leap to where we are today.”

Researchers also found activity as expected in regions of the brain that encode visual and auditory inputs, as well as the parietal lobe, which is known to be involved in numerical and calculation-related functions.

From a practical standpoint, the findings could prove useful in avoiding important areas during surgeries to remove tumors or epilepsy focal points, or in placing neurostimulators designed to stop seizures.

“Brain areas involved in processing numbers can be delineated and extra care taken to avoid damaging these areas during neurosurgical interventions,” said lead author Alexander Rockhill, PhD, a postdoc in Raslan’s lab.

Researchers credited the patients involved in the study.

“We are extremely grateful to our epilepsy patients for their willingness to participate in this research,” said co-author Christian Lopez Ramos, MD, neurosurgical resident at OHSU. “Their involvement in answering our questions during surgery turned out to be the key to advancing scientific understanding about how our brain evolved in the deep past and how it works today.”

Indeed, the study follows previous lines of research involving mapping of the human brain during surgery.

“I have access to the most valuable human data in nature,” Raslan said. “It would be a shame to miss an opportunity to understand how the brain and mind function. All we have to do is ask the right questions.”

In the next stage of this line of research, Raslan anticipates discerning areas of the brain capable of performing other higher-level functions.

Source: Ohio State University

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Intracranial EEG Captures Neurons Resonating as They Turn Words into Thoughts

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The lines on this diagram of the brain represent connections between various areas of the cerebral cortex involved in language processing. When we read, the neurons in these areas fire in precise synchronicity, a phenomenon known as “co-rippling.” Photo credit: UC San Diego Health Sciences

Researchers at University of California San Diego School of Medicine have brought us closer to solving how the brain processes information from specialised areas into a whole. By delving into the brain with intracranial electroencephalography, they observed how neurons synchronise across the human brain while reading. The findings are published in Nature Human Behaviour and are also the basis of a thesis by UC San Diego School of Medicine doctoral candidate Jacob Garrett.

“How the activity of the brain relates to the subjective experience of consciousness is one of the fundamental unanswered questions in modern neuroscience,” said study senior author Eric Halgren, Ph.D., professor in the Departments of Neurosciences and Radiology at UC San Diego School of Medicine. “If you think about what happens when you read text, something in the brain has to turn that series of lines into a word and then associate it with an idea or an object. Our findings support the theory that this is accomplished by many different areas of the brain activating in sync.”

This synchronisation of different brain areas, called “co-rippling” is thought to be essential for binding different pieces of information together to form a coherent whole. In rodents, co-rippling has been observed in the hippocampus, the part of the brain that encodes memories. In humans, Halgren and his colleagues previously observed that co-rippling also occurs across the entire cerebral cortex.

To examine co-rippling at the mechanistic level, Ilya Verzhbinsky, an MD/PhD candidate completing his research in Halgren’s lab, led a study published in PNAS that looked at what happens to single neurons firing in different cortical areas during ripples. The present study looks at the phenomenon with a wider lens, asking how the many billions of neurons in the cortex are able to coordinate this firing to process information.

“There are 16 billion neurons in the cortex – double the number of people on Earth,” said Halgren. “In the same way a large chorus needs to be organised to sound as a single entity, our brain neurons need to be coordinated to produce a single thought or action. Co-rippling is like neurons singing on pitch and in rhythm, allowing us to integrate information and make sense of the world. Unless they’re co-rippling, these neurons have virtually no effect on the other, but once ripples are present about two thirds of neuron pairs in the cortex become synchronised. We were surprised by how powerful the effect was.”

Co-rippling in the cortex has been difficult to observe in humans due to limitations of noninvasive brain scanning. To work around this problem, the researchers used an approach called intracranial electroencephalography (EEG) scanning, which measures the electrical activity of the brain from inside the skull. The team studied a group of 13 patients with drug-resistant epilepsy who were already undergoing EEG monitoring as part of their care.

Participants were shown a series of animal names interspersed with strings of random consonants or nonsense fonts and then asked to press a button to indicate the animal whose name they saw. The researchers observed three stages of cognition during these tests: an initial hierarchical phase in visual areas of the cortex in which the participant could see the word without conscious understanding of it; a second stage in which this information was “seeded” with co-ripples into other areas of the cortex involved in more complex cognitive functions; and a final phase, again with co-ripples, where the information across the cortex is integrated into conscious knowledge and a behavioural response – pressing the button.

The researchers found that throughout the exercise, co-rippling (~100ms-long ~90Hz oscillations) occurred between the various parts of the brain engaged in these cognitive stages, but the rippling was stronger when the participants were reading real words.

The study’s findings have potential long-term implications for the treatment of neurological and psychiatric disorders, such as schizophrenia, which are characterised by disruptions in these information integration processes.

“It will be easier to find ways to reintegrate the mind in people with these disorders if we can better understand how minds are integrated in typical, healthy cases,” added Halgren.

More broadly, the study’s findings have significant implications for our understanding of the link between brain function and human experience.

“This is a fundamental question of human existence and gets at the heart of the relationship between mind and brain,” said Halgren. “By understanding how our brain’s neurons work together, we can gain new insights into the nature of consciousness itself.”

Source: University of California San Diego

Categories : NeurologyTags :

Could a New Role for Propofol be Treating Epilepsy?

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The general anaesthetic propofol may hold the keys to developing new treatment strategies for epilepsy and other neurological disorders, according to a study led by researchers at Weill Cornell Medicine and Linköping University in Sweden.

In their study, published in Nature, the researchers determined the high-resolution structural details of how propofol inhibits the activity of HCN1, an ion channel protein found on many types of neurons. Drug developers consider inhibiting HCN1 a promising strategy for treating neurologic disorders including epilepsy and chronic pain. The researchers also found, to their surprise, that when HCN1 contains either of two epilepsy-associated mutations, propofol binds to it in a way that restores its functionality.

“We might be able to exploit propofol’s unique way of binding to HCN1 for the treatment of these drug-resistant epilepsies and other HCN1-linked disorders, either by directly repurposing propofol or by designing new, more selective drugs that have the same mechanism of action,” said study co-senior author Dr Crina Nimigean, professor of physiology and biophysics in anaesthesiology at Weill Cornell Medicine.

The study’s first author was Dr Elizabeth Kim, a postdoctoral research associate in the Nimigean laboratory.  

HCN ion channels in humans come in four basic forms, HCN1 to HCN4, and are found especially on cells in the heart and nervous system. They work as switches to control the electrical voltage across the cell membrane, opening to admit an inward flow of positively charged potassium and sodium ions – thus “depolarising” the cell – when the voltage reaches a certain threshold. This function underpins much of the rhythmic activity of brain and heart muscle cells, which is why HCN channels are also called pacemaker channels.

In the study, the researchers used cryo-electron microscopy and other methods to determine, at near-atomic scale, how propofol reduces HCN1 activity – which it does with selectivity for HCN1 over other HCNs. They found that the drug inhibits HCN1 by binding within a groove between two elements of the channel protein’s central pore structure, making it harder for the pore to open.

As they investigated propofol’s action on HCN1, the researchers examined how the drug affects different known mutants of the channel, including mutants that leave it excessively open and are associated with hard-to-treat epilepsy syndromes such as early infantile epileptic encephalopathy (EIEE). The researchers were surprised to find that for two different HCN1 mutations that cause EIEE, propofol restores the mutant channels to normal or near-normal function.

From their experiments, the researchers derived a model in which the mutations decouple HCN1’s voltage-sensing and pore mechanisms, while propofol effectively recouples them, allowing membrane voltage to control ion flow again.

The results suggest at least two possibilities for translation to therapies. One is simply to use propofol, an existing, approved drug, to treat these HCN1-mutation epilepsies and potentially other HCN1-linked disorders. Propofol is a potent anesthetic that requires careful monitoring by anaesthesiologists, but it might be able to restore HCN1 function at doses below those used for general anaesthesia.

The other possibility, the researchers said, is to use the new structural data on propofol’s binding to design modified, non-anesthetic versions of propofol, or even completely different compounds, that bind to HCN1 with a similar effect but much more selectively—in other words, without binding to other channels, including other HCNs, in the body and thereby potentially causing unwanted side effects.

“For that we will need a better understanding of how propofol inhibits HCN1 better than other HCN channels,” Dr Kim said.

Source: Weill Cornell Medicine

Categories : Implants and Prostheses NeurologyTags :

New Neural Prosthetic Device Can Help Restore Memory in Humans

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Scientists have demonstrated the first successful use of a neural prosthetic device to recall specific memories. The findings appear online in Frontiers in Computational Neuroscience.

This groundbreaking research was derived from a 2018 study led by Robert Hampson, PhD, professor of regenerative medicine, translational neuroscience and neurology at Wake Forest University School of Medicine. That study demonstrated the successful implementation of a prosthetic system that uses a person’s own memory patterns to facilitate the brain’s ability to encode and recall memory, improving recall by as much as 37%.

In the previous study, the team’s electronic prosthetic system was based on a multi-input multi-output (MIMO) nonlinear mathematical model, and the researchers influenced the firing patterns of multiple neurons in the hippocampus, a part of the brain involved in making new memories.

In this study, researchers from Wake Forest and University of Southern California (USC) built a new model of processes that assists the hippocampus in helping people remember specific information.

When the brain tries to store or recall information such as, “I turned off the stove” or “Where did I put my car keys?” groups of cells work together in neural ensembles that activate so that the information is stored or recalled.

Using recordings of the activity of these brain cells, the researchers created a memory decoding model (MDM) which let them decode what neural activity is used to store different pieces of specific information.

The neural activity decoded by the MDM was then used to create a pattern, or code, which was used to apply neurostimulation to the hippocampus when the brain was trying to store that information.

“Here, we not only highlight an innovative technique for neurostimulation to enhance memory, but we also demonstrate that stimulating memory isn’t just limited to a general approach but can also be applied to specific information that is critical to a person,” said Brent Roeder, Ph.D., a research fellow in the department of translational neuroscience at Wake Forest University School of Medicine and the study’s corresponding author.

The team enrolled 14 adults with epilepsy who were participating in a diagnostic brain-mapping procedure that used surgically implanted electrodes placed in various parts of the brain to pinpoint the origin of their seizures.

Participants underwent all surgical procedures, post-operative monitoring and neurocognitive testing at one of the three sites participating in this study including Atrium Health Wake Forest Baptist Medical Center, Keck Hospital of USC in Los Angeles and Rancho Los Amigo National Rehabilitation Center in Downey, California.

The team delivered MDM electrical stimulation during visual recognition memory tasks to see if the stimulation could help people remember images better.

They found that when they used this electrical stimulation, there were significant changes in how well people remembered things. In about 22% of cases, there was a noticeable difference in performance.

When they looked specifically at participants with impaired memory function, who were given the stimulation on both sides of their brain, almost 40% of them showed significant changes in memory performance.

“Our goal is to create an intervention that can restore memory function that’s lost because of Alzheimer’s disease, stroke or head injury,” Roeder said.

“We found the most pronounced change occurred in people who had impaired memory.”

Roeder said he hopes the technology can be refined to help people live independently by helping them recall critical information such as whether medication has been taken or whether a door is locked.

“While much more research is needed, we know that MDM-based stimulation has the potential to be used to significantly modify memory,” Roeder said.

Source: Atrium Health Wake Forest Baptist

Categories : Ageing Diseases, Syndromes and ConditionsTags :

Promising Results for Epilepsy Drug in Slowing Osteoarthritis

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Yale researchers report in the journal Nature that they have identified a drug target that may alleviate joint degeneration associated with osteoarthritis.

The most common therapies for the degenerative disease have been pain relievers and lifestyle changes, to reduce pain and stiffness, but there is a pressing need for therapies that can prevent joint breakdown that occurs in osteoarthritis, which occurs as a result of the breakdown of cartilage in the joints.

Sodium channels found in cell membranes produce electrical impulses in “excitable” cells within muscles, the nervous system, and the heart. And in previous research, Yale’s Stephen G. Waxman identified the key role of one particular sodium channel, called Nav1.7, in the transmission of pain signals.

Now, the labs of Chuan-Ju Liu, professor of orthopaedics, and Waxman, professor neurology, neuroscience and pharmacology, have found that the same Nav1.7 channels are also present in non-excitable cells that produce collagen and help maintain the joints in the body. These channels can be targeted by existing drugs to block them.

In the new study, the researchers deleted Nav1.7 genes from these collagen-producing cells and significantly reduced joint damage in two osteoarthritis models in mice.

They also demonstrated that drugs used to block Nav1.7 – including carbamazepine, a sodium channel blocker currently used to treat epilepsy and trigeminal neuralgia – also provided substantial protection from joint damage in the mice.

“The function of sodium channels in non-excitable cells has been a mystery,” Waxman said.

“This new study provides a window on how small numbers of sodium channels can powerfully regulate the behaviour of non-excitable cells.”

“The findings open new avenues for disease-modifying treatments,” added Wenyu Fu, a research scientist in the Liu laboratory and first author of the study.

Source: Yale University

Categories : NeurologyTags :

What Happens When the Brain Loses a Hub?

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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