Category: Neurology

Categories : NeurologyTags :

Most Epilepsy Patients Wait a Year After Starting Treatment for Seizure Relief

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Source: Pixabay

Antiseizure medications help the majority of people with focal epilepsy, a common form of the neurological disorder. Yet most will still have episodes for at least a year after their treatment begins, until their doctors can find the right drug and dosage for them, a new study shows.

Accounting for about 60% of people with epilepsy, focal epilepsy occurs when nerve cells in a certain brain region send out a sudden, excessive burst of electrical signals. This uncontrolled activity, which is called a focal seizure, can cause problems such as abnormal emotions or feelings and unusual behaviours. Much attention has been paid to the minority of patients who do not respond well to available treatments, but the current study looks at another group: those who may not respond to the first medication or regimen prescribed but who might respond to another tried later.

Led by researchers at NYU Langone Health as part of the international Human Epilepsy Project, the study is among the first in a decade to focus on those whose seizures ultimately can be prevented or controlled with drugs. Results for nearly 450 men, women, and teens newly diagnosed with the disorder revealed that although more than half eventually received a medication or regimen that worked for them, major improvements were not achieved until an average of 12 months. Many needed even longer to find relief.

“Our findings suggest that those with focal epilepsy should expect a long adjustment period as their healthcare provider determines the best treatment regimen for them,” said study senior author and neurologist Jacqueline A. French, MD.

A possible explanation for this delay is that physicians are not selecting the ideal antiseizure therapy on their first try, adds Dr French, a professor in the Department of Neurology at the NYU Grossman School of Medicine and co-principal investigator of the Human Epilepsy Project.

Neurologists commonly start patients on levetiracetam, a drug that can target many types of seizures and has few interactions with other medications. Based on the new results, however, they may want to rethink this approach, says Dr French, noting that although 57% of the study participants were initially prescribed levetiracetam, only a quarter became seizure free on their first try.

A report on the findings appears in JAMA Neurology.

Thirty-four epilepsy centres in the United States, Europe, and Australia were involved in the study, which took place from 2012 to 2019. The team collected data about the patients’ medical histories, demographic factors, and the details of their epilepsy diagnoses. All were provided annual follow-ups for either three or six years.

During this time, participants tracked their seizure frequency in an electronic diary, describing each day as either “seizure-free” or “had a seizure.” The time, duration, and type of episode, along with other notes, were also recorded. The study volunteers also reported information about their antiseizure medications, noting the type, dose, and reasons for discontinuing a regimen.

Patients were considered seizure-free if they did not have an episode for at least a year (or longer if their seizures were infrequent).

The study further showed that together, 63% of all participants experienced ongoing or even worsening seizures during the first year of therapy, whether or not they would eventually find relief.

Notably, those who had seizures only a few times per year prior to treatment were more likely to respond to medication than those who had them weekly. In addition, participants with a history of psychological disorders such as anxiety and depression were almost twice as likely to resist the drugs than those without such a history.

“Our results show that the best way to a new treatment plan is sometimes through making better use of the tools we already have instead of always searching for the next breakthrough drug,” said Dr French, who is also a member of NYU Langone’s Comprehensive Epilepsy Center.

The researchers next plan to more closely examine those who did not become seizure-free during the study period, says Dr French.

Dr French cautions that the investigation did not directly assess the role of regimen choice, dose, or side effects on the way patients responded to treatment, and it did not exclude participants who failed to adhere to their prescribed regimen.

Source: NYU Langone Health

Categories : NeurologyTags :

Scientists Repair Stroke Damage in Mice Using Stem Cells

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This image shows a coronal section through the mouse brain after stroke and neural stem cell transplantation. The dashed circle indicates the stroke area. The neurite projections of the transplanted human cells are stained in dark brown. Neurites extend locally into the cortex (CX) but also via the corpus callosum (CC) into the other brain hemisphere. (Image: UZH)

One in four adults suffer a stroke in their lifetime, leaving around half of them with residual damage such as paralysis or speech impairment because internal bleeding or a lack of oxygen supply kill brain cells irreversibly. No therapies currently exist to repair this kind of damage. “That’s why it is essential to pursue new therapeutic approaches to potential brain regeneration after diseases or accidents,” says Christian Tackenberg, the Scientific Head of Division in the Neurodegeneration Group at the University of Zurich (UZH) Institute for Regenerative Medicine.

Neural stem cells have the potential to regenerate brain tissue, as a team led by Tackenberg and postdoctoral researcher Rebecca Weber has now compellingly shown in two studies that were conducted in collaboration with a group headed by Ruslan Rust from the University of Southern California. “Our findings show that neural stem cells not only form new neurons, but also induce other regeneration processes,” Tackenberg says.

The first study is published in Nature Communications, the second in Science Advances.

New neurons from stem cells

The studies employed human neural stem cells, from which different cell types of the nervous system can form. The stem cells were derived from induced pluripotent stem cells, which in turn can be manufactured from normal human somatic cells. For their investigation, the researchers induced a permanent stroke in mice, the characteristics of which closely resemble manifestation of stroke in humans. The animals were genetically modified so that they would not reject the human stem cells.

One week after stroke induction, the research team transplanted neural stem cells into the injured brain region and observed subsequent developments using a variety of imaging and biochemical methods. “We found that the stem cells survived for the full analysis period of five weeks and that most of them transformed into neurons, which actually even communicated with the already existing brain cells,” Tackenberg says.

Brain regenerates itself

The researchers also found other markers of regeneration: new formation of blood vessels, an attenuation of inflammatory response processes and improved blood-brain barrier integrity. “Our analysis goes far beyond the scope of other studies, which focused on the immediate effects right after transplantation,” Tackenberg explains. Fortunately, stem cell transplantation in mice also reversed motor impairments caused by stroke. Proof of that was delivered in part by an AI-assisted mouse gait analysis.

Clinical application moving closer to reality

Human neural stem cells in culture. Cell nuclei are stained in blue, the neural stem cell-specific filament protein Nestin is shown in green, and the neural stem cell transcription factor Sox1 in red. (Image: UZH)

When he was designing the studies, Tackenberg already had his sights set on clinical applications in humans. That’s why, for example, the stem cells were manufactured without the use of reagents derived from animals. The Zurich-based research team developed a defined protocol for that purpose in collaboration with the Center for iPS Cell Research and Application (CiRA) at Kyoto University. This is important for potential therapeutic applications in humans. Another new insight discovered was that stem cell transplantation works better when it is performed not immediately after a stroke but a week later, as the second study verified. In the clinical setting, that time window could greatly facilitate therapy preparation and implementation.

Despite the encouraging results of the studies, Tackenberg warns that there is still work to be done. “We need to minimize risks and simplify a potential application in humans,” he says. Tackenberg’s group, again in collaboration with Ruslan Rust, is currently working on a kind of safety switch system that prevents uncontrolled growth of stem cells in the brain. Delivery of stem cells through endovascular injection, which would be much more practicable than a brain graft, is also under development. Initial clinical trials using induced stem cells to treat Parkinson’s disease in humans are already underway in Japan, Tackenberg reports. “Stroke could be one of the next diseases for which a clinical trial becomes possible.”

Source: University of Zurich

Categories : Cardiovascular Disease NeurologyTags :

Landmark Study Finds Perispinal Etanercept of No Benefit to Stroke Trial Participants

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A treatment for stroke patients was no more effective than an inactive drug

Source: CC0

The first international trial of an unproven stroke treatment available in the US has concluded that, while harmless, perispinal etanercept is no more effective than an inactive dummy drug, or placebo.

Survivors of stroke have travelled at considerable expense to private clinics in the US to be treated with the arthritis drug etanercept.

In the clinics, the drug is injected into the cervical spinal area, and the patient is then tilted head-down in the belief that this allows the drug to enter the brain.

Stroke is a leading cause of disability throughout the world, affecting more than 7 million people a year. Despite advances, treatments for impairment after stroke remain limited. Some patients call perispinal etanercept a “miracle cure”.

Florey leading stroke researcher, neurologist Professor Vincent Thijs led the Perispinal Etanercept to improve STroke Outcomes – or “PESTO” – trial to investigate this further, supported by funding from the Australian Government.

“We understand why people living with the long-term effects of stroke seek hope and new options,” Professor Thijs said. “With support from the Stroke Foundation and the Medical Research Future Fund, we put this treatment to the test using the gold standard of clinical research – a double-blind randomised trial.”

Half of the PESTO participants were treated with the drug, and half were treated with an inactive dummy drug, with patients and doctors “blind” to who was getting which.

This type of trial eliminates biases because neither doctors nor patients knew who was getting etanercept and who was getting the placebo. Because the results for the 2 patient groups were so similar, we concluded that while the drug did not cause harm, we found no evidence that it led to improved quality of life compared to placebo.

Professor Thijs, who leads the Young Stroke Service at The Florey, said improvements could be due to the placebo effect, a well-established medical phenomenon where some patients in a trial may notice an improvement, despite only receiving a dummy treatment.

Key PESTO trial results, published in Neurology:

  • 126 people from Australia and New Zealand participated in PESTO.
  • 63 received the treatment, 63 the placebo.
  • Their stroke symptoms were measured before the trial and 28 days after.
  • There were no adverse side effects.
  • Among participants who received perispinal etanercept, 52 per cent (33 out of 63) felt better.
  • Among participants who received the placebo, 57 per cent (36 out of 63) felt better.
  • The difference in results between the 2 groups is deemed statistically insignificant.

“It’s important for doctors and the stroke survivor community in Australia and around the world to know that we found no evidence that perispinal etanercept improved quality of life,” Professor Thijs said.

Kelvin Hill, Executive Director of Stroke Programs, Research and Innovation at Stroke Foundation said: “Every Australian stroke patient should have access to the best, evidence-based treatment. Findings of the PESTO study underscore the critical importance of robust research and clinical trials in discovering if treatments work or not.

“Australians experience around 46 000 stroke events every year (one every 11 minutes), and there are now over 440 000 survivors of stroke living in Australia. Stroke Foundation will continue to advocate for more research funding to unlock new effective treatments for stroke; and ensure that advice provided in the Living Clinical Guidelines for Stroke Management enables clinicians to provide the best stroke care possible,” Mr Hill added.

Source: Florey Institute of Neuroscience and Mental Health

Categories : NeurologyTags :

Oxytocin Shines a Light into Parental Attachment and Sex Differences

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The developing brain of a two-week-old mouse pup under the microscope. The oxytocin system appears in green, the light-sensitive protein in red and cells that carry both show up in yellow. Cell nuclei are in blue. Credit: Weizmann Institute of Science

According to attachment theory, the attachment between an infant and a primary caregiver shapes the baby’s future social ties. Yet little is known about the biological mechanisms underlying childhood attachment, mainly because it is so difficult to study the young brain in natural conditions.

Now, scientists in Prof Ofer Yizhar’s laboratory at the Weizmann Institute of Science have developed a new, noninvasive research method that makes it possible to silence selected nerve cells deep within the brains of mouse pups without disrupting their natural behaviour. Using this method, the researchers investigated the role of oxytocin, a short protein released from nerve cells in the brain. While most oxytocin research has focused on adults, the new findings, published in Science, show that oxytocin also shapes the social behaviour of pups and may underlie emotional differences between males and females that emerge early in life.

Oxytocin, sometimes referred to as the “love hormone,” was once thought to simply promote sociability in adults. Over time, however, it became clear that its role is far more complex: In some circumstances, it intensifies behaviors and emotions far removed from love, such as anxiety or aggression. Recent research has also shown that young mammalian brains – including those of human children – are especially sensitive to oxytocin. In brain regions responsible for sensory processing, emotional regulation and social behavior, the number of oxytocin receptors peaks during early childhood: around ages two to three in humans, and two to three weeks in mice. Some studies have even linked oxytocin deficiency to childhood autism. Still, without sufficiently precise tools to examine neural activity deep within the developing brain, many aspects of the role of oxytocin in early life have remained a mystery.

“The findings may offer a clue as to why males and females diverge in their social behaviors and emotional worlds long before puberty”

To shed light on the subject, a team led by Dr Daniel Zelmanoff, a physician-scientist in Yizhar’s lab, developed a noninvasive technique to probe specific nerve cells in the young brain. The group, pioneers in the field of optogenetics – a technology that uses light to switch individual cells on or off – devised a method in which the targeted brain cells of mouse pups are infected with an engineered virus. This otherwise harmless virus introduces a foreign gene of mosquito origin that encodes a light-sensitive protein; when exposed to light, the protein “turns off” the nerve cell. In fact, the protein is so light-sensitive that the researchers could silence selected nerve cells deep inside the brain simply by shining red light on the pups’ heads.

“This new method allows us to peek inside the brain without disturbing the pups’ everyday lives, making it a powerful tool for studying nervous system development,” Yizhar explains. “It is especially useful for studying oxytocin because this hormone’s effects depend on social context – and our method lets us switch off the oxytocin system on demand, only during the exact situation we want to study.”

The researchers focused on oxytocin’s role during the temporary separation of a mouse pup from its mother and their reunion a few hours later – a situation familiar to every parent of a young child. The scientists observed increased oxytocin activity in the pup’s brain during separation, which returned to normal after reunion with the mother. Pups with an active oxytocin system during the separation gradually adapted to being alone in an unfamiliar environment, producing fewer ultrasonic vocalizations – the mouse equivalent of a baby’s cry. In contrast, pups whose oxytocin system was silenced did not adapt; they continued emitting distress calls at the same rate until reunited with their mothers. These findings show that the so-called “love hormone” also plays a critical role in coping with loneliness.

Attachment theory holds that children who are securely attached to their parents show distress when separated from them but are able to calm down over time, feeling free to explore their surroundings. “We discovered that mouse pups need an active oxytocin system in order to adapt to separation from their mothers,” says Yizhar. “This suggests that the oxytocin system plays a role not only in the brain of the parent, which was already known, but also in that of the infant. In addition, since oxytocin receptors are present in the sensory processing centers of the young brain, we hypothesize that this hormone also helps sharpen a pup’s senses when it is alone.”

Children do not quickly forget the experience of being separated from their parents, and this separation shapes how they behave when reunited. For example, a securely attached child separated from a parent for a few hours will seek contact upon reunion, and is quickly calmed. The researchers found that activation of the oxytocin system in mouse pups during separation not only strengthened them in the moment but also determined how they behaved when their mothers returned. These pups emitted more ultrasonic calls than usual, and the frequency of the calls grew as they got closer to their mothers. Using artificial intelligence, the team identified a distinct vocal pattern: Before attaching to the mother’s nipple, the pups made high-pitched, frequent calls; afterwards, their calls dropped in pitch and slowed in tempo.

“Activating the oxytocin system during separation increases the pup’s motivation to regain closeness to the mother when reunited,” Yizhar explains. “This is reflected in the heightened rate and unique pattern of their calls. We now understand that these ultrasonic vocalizations are much more than just crying: The high-pitched, rapid calls appear to signal a request for closeness, while the lower-pitched, slower-paced calls likely express a quick return to calm and a wish to remain attached. Of course, more research is needed to pin down the exact meaning of each vocalization type.”

In the next stage, the researchers explored whether oxytocin’s role in pups differs between the sexes, as it does in older animals. They found that female pups with an active oxytocin system emitted many more ultrasonic calls when reunited with their mothers than females with silenced oxytocin systems, whereas the calls of male pups were unaffected by the status of their oxytocin systems. “This is the first sex difference observed in oxytocin system activity at such an early stage of development,” Yizhar notes. “It may offer a clue as to why males and females diverge in their social behaviours and emotional worlds long before puberty.”

“Most known functions of oxytocin are shared by all mammals,” Yizhar concludes. “Still, future studies must check whether the hormone affects the development of social behaviour, emotional maturity and maternal attachment in the brains of children. If so, this could help us better understand what can go wrong in emotional and social development – as in autism spectrum disorder, for example – and how to intervene at an early stage.”

Source: Weizmann Institute of Science

Categories : Neurology Substance UseTags :

Brain Study Prompts a Rethink of Alcohol Abuse and Relapse

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Photo from Pixabay CC0

What compels someone to keep engaging in alcohol use, even if it damages their health, relationships and wellbeing? A new study from Scripps Research offers an important clue: a small midline brain region plays a key role in how animals learn to continue drinking to avoid the stress and misery of withdrawal.

In a new study, published in Biological Psychiatry: Global Open Science on August 5, 2025, the Scripps Research team zeroed in on a set of brain cells in the paraventricular nucleus of the thalamus (PVT) in rats. They found that this region becomes more active, driving strong relapse behaviour, when rats learn to associate environmental stimuli with the easing of withdrawal symptoms by alcohol. By illuminating this brain pathway, the research sheds light on one of the most stubborn features of addiction – drinking not for pleasure, but to escape pain – and could eventually lead to new treatments for substance use disorders (SUDs) as well as other maladaptive behaviours including anxiety. 

“What makes addiction so hard to break is that people aren’t simply chasing a high,” says Friedbert Weiss, professor of neuroscience at Scripps Research and senior author of the study. “They’re also trying to get rid of powerful negative states, like the stress and anxiety of withdrawal. This work shows us which brain systems are responsible for locking in that kind of learning, and why it can make relapse so persistent.”

“This brain region just lit up in every rat that had gone through withdrawal-related learning,” says co-senior author Hermina Nedelescu of Scripps Research. “It shows us which circuits are recruited when the brain links alcohol with relief from stress – and that could be a game-changer in how we think about relapse.”

From behaviour to brain maps

An estimated 14.5 million people in the United States have alcohol use disorder, which encompasses a range of unhealthy drinking behaviours. Like other drug addictions, alcohol addiction is characterised by cycles of withdrawal, abstinence and relapse. 

In 2022, Weiss and Nedelescu used rats to study the types of learning that happen in the brain throughout this cycle. When rats initially begin drinking, they learn to associate pleasure with alcohol and seek more. However, that conditioning becomes far stronger during multiple cycles of withdrawal and relapse. After learning that alcohol eased the unpleasant feelings of withdrawal – negative reinforcement, or a relief of ‘negative hedonic state’ – the animals sought out more alcohol and would remain persistent even when uncomfortable.

“When rats learn to associate environmental stimuli or contexts with the experience of relief, they end up with an incredibly powerful urge to seek alcohol in the presence of that stimuli –even if conditions are introduced that require great effort to engage in alcohol seeking,” says Weiss. “That is, these rats seek alcohol even if that behavior is punished.” 

In the new work, the team wanted to pin down exactly what networks of cells in the brain were responsible for learning to associate environmental cues with the relief of this negative hedonic state.

The researchers used advanced imaging tools to scan entire rat brains, cell by cell, and pinpoint areas that became more active in response to alcohol-related cues. They compared four groups of rats: those that had gone through withdrawal and learned that alcohol relieves a negative hedonic state, and three different control groups that had not.

While several brain areas showed increased activity in the withdrawal-learned rats, one stood out: the PVT, which is known for its role in stress and anxiety.

“In retrospect, this makes a lot of sense,” says Nedelescu. “The unpleasant effects of alcohol withdrawal are strongly associated with stress, and alcohol is providing relief from the agony of that stressful state.” 

The researchers hypothesise that this negative hedonic state, and the activation of the PVT in the brain as a response, is critical for how the brain learns and perpetuates addiction.

A better understanding of addiction

The implications of the new study extend well beyond alcohol, the researchers say. Environmental stimuli conditioned to negative reinforcement – the drive to act in order to escape pain or stress – is a universal feature of the brain, and can drive human behaviour beyond substance use disorders such as anxiety disorders, fear-conditioning and traumatic avoidance learning.

“This work has potential applications not only for alcohol addiction, but also other disorders where people get trapped in harmful cycles,” says Nedelescu.

Future research will zoom in even further. Nedelescu and colleagues at Scripps Research want to expand the study to females and to study neurochemicals released in the PVT when subjects encounter environments associated with the experience of this relief from a negative hedonic state. If they can pinpoint molecules that are involved, it could open new avenues for drug development by targeting those molecules.

For now, the new study underscores a key shift in how basic scientists think about addiction.

 “As psychologists, we’ve long known that addiction isn’t just about chasing pleasure – it’s about escaping those negative hedonic states,” says Weiss. “This study shows us where in the brain that learning takes root, which is a step forward.”

Source: Scripps Research

Categories : Exercise NeurologyTags :

More Research Shows that Yoga May Also Protect Brain Health

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Photo by RDNE Stock project

Anyone who has taken a yoga class knows how relaxing it can be to set aside the day’s worries and focus on breathing, gentle movements, healing stretches and guided meditation, even if just for an hour.

A growing body of research suggests the soothing powers of yoga may go further than temporarily easing the day’s stress. Yoga is emerging as a potential prescription to boost brain power, offset cognitive decline and help prevent dementia.

“The evidence behind yoga has really picked up,” said Dr Neha Gothe, an associate professor and director of the PhD in Human Movement and Rehabilitation Sciences programme at Bouvé College of Health Sciences at Northeastern University in Boston. “So far, it points toward the potential for it to protect brain health as we are aging.”

Exercise for an aging brain

Research into the health benefits of yoga – the origins of which trace back to 2500 to 5000 years ago – didn’t begin in earnest until the 2000s, when the practice began to surge in popularity in the US, Gothe said. Since then, yoga practice has been shown to have a positive influence on physical as well as mental health, with studies finding it may benefit cardiovascular function, musculoskeletal conditions and overall mental well-being.

More recently, researchers have turned their attention to yoga’s potential benefits on brain health, an area of growing interest as the population ages and the number of adults developing dementia and cognitive decline rises. In the U.S., about 1 in 5 people 65 and older are living with mild cognitive impairment, and 1 in 7 have some type of dementia. Researchers predict a doubling of new dementia cases in the U.S. over the next several decades.

While there is strong evidence that physical activity can benefit brain health and help slow cognitive decline, aging adults are not always able to reach the recommended 150 minutes of moderate-intensity exercise or 75 minutes of vigorously intense physical activity needed to reap these benefits. Federal guidelines also recommend muscle-strengthening activities at least two days a week.

What the research shows about yoga

Yoga – which combines physical movement with breath work and meditation – may offer a more accessible alternative or supplement to other types of exercise, Gothe said.

Studies have shown yoga may have a positive effect on both brain structure and function. In a 2019 analysis of the evidence, Gothe found yoga could hold promise as a means of offsetting age-related and neurodegenerative declines in several regions of the brain. And in another small study comparing yoga practitioners to age- and sex-matched controls, she found women who practiced yoga regularly had more grey matter – the part of the brain that controls memory, thought and movement – and better working memory than those who didn’t.

In some cases, the ancient practice may even be better for the brain than other types of physical activity. In another small study, Gothe found cancer survivors who practiced yoga for 12 weeks reported greater cognitive improvement than those who engaged in aerobic and stretching-toning exercises.

For people who can’t engage in more vigorous activities, it’s certainly more accessible, Gothe said.

“Yoga is just as good as any other form of physical activity, such as walking or stretching,” she said. “For individuals who may not be able to engage in those activities, especially older adults who have other conditions, such as knee pain or arthritis, yoga is a neat alternative to traditional forms of exercise and is very modifiable to accommodate an individual’s abilities.”

How does yoga help?

An explanation for yoga’s brain health benefits may be the close connection yoga forms between the mind and body.

Gothe and her colleagues found the cognitive benefits of yoga may stem from limiting prolonged exposure to stress and inflammation, improving stress regulation and helping the brain communicate better with the body to work more efficiently.

“We have a lot of evidence at this point telling a cohesive story about a mind-body connection with brain health,” said Dr Helen Lavretsky, a professor of psychiatry in-residence and director of integrative psychiatry at the David Geffen School of Medicine at the University of California, Los Angeles.

Lavretsky has led numerous studies on the cognitive benefits of yoga, looking specifically at Kundalini yoga. This type of yoga blends physical postures with meditation and breathing techniques that focus on relaxation, healing and self-awareness.

In several studies, Lavretsky’s team compared Kundalini yoga to memory enhancement training in postmenopausal women: those who practised yoga experienced greater improvements in memory and cognitive function, including executive function, and were able to better prevent grey matter atrophy.

In a separate analysis of published research, Lavretsky looked more broadly at mind-body practices, including yoga and meditation. The review suggested that these practices improved brain function because they were targeting the area of the brain involved in regulating attention, emotional control, mood and cognition.

“Yoga and other mind-body therapies have an effect on stress reduction and other things that underlie brain health,” Lavretsky said. “Our research shows they are well equipped to reduce inflammation, stress, improve sleep and mental health.”

Making yoga a regular practice

How much and what type of yoga is needed to accrue these benefits remains unclear.

While Lavretsky’s studies involved Kundalini yoga, Gothe said her studies mostly involved Hatha yoga, the most widely practiced form. Both blend physical postures with breathing exercises, while Kundalini incorporates more spiritual and meditation elements.

Most studies involve at least eight weeks of yoga, with hourlong classes at least two or three times a week, Gothe said. But “there are no rigorous dose-response studies. So we don’t know exactly what dose is necessary to get an improvement in cognitive performance.”

Even so, yoga shouldn’t be considered a quick fix, Gothe said. To maintain benefits, it’s important to keep up the practice.

“It is a ‘use it or lose it’ phenomena,” she said. “If you continue practicing, you will continue to see improvement. But if you stop, you go back to square one.”

The good news is it’s never too late to begin accruing those benefits, Lavretsky said. She encourages people to begin at a young age, so they have a tool for stress management whenever it’s needed.

“The benefit of starting earlier is that it becomes a lifelong skill,” she said. “But yoga has benefits no matter what your age is.”

Source: American Heart Association

Categories : NeurologyTags :

New Ultrasound Helmet Enables Deep Brain Stimulation in People Without Surgery

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Illustration of new ultrasound device. Credit: Morgan Roberts.

Scientists have long been looking for a way to modulate brain function, which could improve our understanding of how the brain works and help to treat neurological diseases, using non-invasive methods that don’t involve surgery.

One technology that could help is transcranial ultrasound stimulation (TUS), which was recently discovered to be able to modulate the activity of neurons (the brain’s key communication cells) by delivering gentle mechanical pulses that influence how these cells send signals.

But to date current systems have struggled to reach deeper areas of the brain with sufficient precision to target specific brain structures. Conventional TUS systems often affect broader regions than intended, limiting their utility for targeted neuromodulation.

The study, published in Nature Communications, introduces a new ultrasound device capable of influencing deep brain regions without surgery for the first time, targeting areas around 1000 times smaller than conventional ultrasound devices can pinpoint and 30 times smaller than previous deep brain ultrasound devices.

The new technology features 256 elements configured within a special helmet to send focused beams of ultrasound to specific parts of the brain in order to turn neuronal activity up or down. It also includes a soft plastic face mask which helps to target the ultrasound waves more precisely by keeping the head still.

The research team demonstrated the system’s capabilities on seven human volunteers by targeting a part of the thalamus, a small structure in the centre of the brain that helps to relay sensory and motor information, called the lateral geniculate nucleus (LGN). The LGN is involved in processing visual information.

In the first experiment, participants looked at a flashing checkerboard, which sent signals to the brain through the eyes. During stimulation with the ultrasound device, a functional magnetic resonance imaging (fMRI) scan showed significantly increased activity in the participants’ visual cortex, confirming precise targeting of the LGN.

A second experiment revealed sustained decreases in visual cortex activity for at least 40 minutes after ultrasound stimulation, highlighting the system’s potential for inducing lasting changes in brain function.

Though participants did not consciously perceive any changes in what they were seeing during the experiments, the brain scans revealed significant changes in neural activity. The ultimate goal is to harness these effects to produce clinically beneficial outcomes, such as stopping hand tremors.

Professor Bradley Treeby, senior author of the study from UCL Medical Physics and Biomedical Engineering, said: “This advance opens up opportunities for both neuroscience research and clinical treatment. For the first time, scientists can non-invasively study causal relationships in deep brain circuits that were previously only accessible through surgery.

“Clinically, this new technology could transform treatment of neurological and psychiatric disorders like Parkinson’s disease, depression, and essential tremor, offering unprecedented precision in targeting specific brain circuits that play key roles in these conditions.

“The ability to precisely modulate deep brain structures without surgery represents a paradigm shift in neuroscience, offering a safe, reversible, and repeatable method for both understanding brain function and developing targeted therapies.”

In addition to its research applications, the system could pave the way for new clinical interventions. Deep brain stimulation (DBS), currently used to treat conditions like Parkinson’s disease, requires invasive surgery and carries associated risks. The new ultrasound system offers a non-invasive alternative with comparable precision, potentially allowing clinicians to test areas of the brain that could be used to treat disease before surgery or even replace surgical approaches altogether.

Recognising this clinical potential, several members of the research team have recently founded NeuroHarmonics, a UCL spinout company developing a portable, wearable version of the system. The company aims to make precise, non-invasive deep brain therapy accessible for both clinical treatment and broader therapeutic applications.

Dr Eleanor Martin, first author of the study from UCL Medical Physics and Biomedical Engineering, said: “We designed the system to be compatible with simultaneous fMRI, enabling us to monitor the effects of stimulation in real time. This opens up exciting possibilities for closed-loop neuromodulation and personalised therapies.”

The researchers emphasise that further studies are needed to fully understand the mechanisms underlying TUS-induced neuromodulation. However, the results mark a significant milestone in the development of safe, effective, and targeted brain stimulation technologies.

Source: University College London

Categories : NeurologyTags :

How ‘Brain Cleaning’ While We Sleep May Lower Our Risk of Dementia

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Photo by Cottonbro on Pexels

Julia Chapman, Macquarie University; Camilla Hoyos, Macquarie University, and Craig Phillips, Macquarie University

The brain has its own waste disposal system – known as the glymphatic system – that’s thought to be more active when we sleep.

But disrupted sleep might hinder this waste disposal system and slow the clearance of waste products or toxins from the brain. And researchers are proposing a build-up of these toxins due to lost sleep could increase someone’s risk of dementia.

There is still some debate about how this glymphatic system works in humans, with most research so far in mice.

But it raises the possibility that better sleep might boost clearance of these toxins from the human brain and so reduce the risk of dementia.

Here’s what we know so far about this emerging area of research.

Why waste matters

All cells in the body create waste. Outside the brain, the lymphatic system carries this waste from the spaces between cells to the blood via a network of lymphatic vessels.

But the brain has no lymphatic vessels. And until about 12 years ago, how the brain clears its waste was a mystery. That’s when scientists discovered the “glymphatic system” and described how it “flushes out” brain toxins.

Let’s start with cerebrospinal fluid, the fluid that surrounds the brain and spinal cord. This fluid flows in the areas surrounding the brain’s blood vessels. It then enters the spaces between the brain cells, collecting waste, then carries it out of the brain via large draining veins.

Scientists then showed in mice that this glymphatic system was most active – with increased flushing of waste products – during sleep.

One such waste product is amyloid beta (Aβ) protein. Aβ that accumulates in the brain can form clumps called plaques. These, along with tangles of tau protein found in neurons (brain cells), are a hallmark of Alzheimer’s disease, the most common type of dementia.

In humans and mice, studies have shown that levels of Aβ detected in the cerebrospinal fluid increase when awake and then rapidly fall during sleep.

But more recently, another study (in mice) showed pretty much the opposite – suggesting the glymphatic system is more active in the daytime. Researchers are debating what might explain the findings.

So we still have some way to go before we can say exactly how the glymphatic system works – in mice or humans – to clear the brain of toxins that might otherwise increase the risk of dementia.

Does this happen in humans too?

We know sleeping well is good for us, particularly our brain health. We are all aware of the short-term effects of sleep deprivation on our brain’s ability to function, and we know sleep helps improve memory.

In one experiment, a single night of complete sleep deprivation in healthy adults increased the amount of Aβ in the hippocampus, an area of the brain implicated in Alzheimer’s disease. This suggests sleep can influence the clearance of Aβ from the human brain, supporting the idea that the human glymphatic system is more active while we sleep.

This also raises the question of whether good sleep might lead to better clearance of toxins such as Aβ from the brain, and so be a potential target to prevent dementia.

How about sleep apnoea or insomnia?

What is less clear is what long-term disrupted sleep, for instance if someone has a sleep disorder, means for the body’s ability to clear Aβ from the brain.

Sleep apnoea is a common sleep disorder when someone’s breathing stops multiple times as they sleep. This can lead to chronic (long-term) sleep deprivation, and reduced oxygen in the blood. Both may be implicated in the accumulation of toxins in the brain.

Sleep apnoea has also been linked with an increased risk of dementia. And we now know that after people are treated for sleep apnoea more Aβ is cleared from the brain.

Insomnia is when someone has difficulty falling asleep and/or staying asleep. When this happens in the long term, there’s also an increased risk of dementia. However, we don’t know the effect of treating insomnia on toxins associated with dementia.

So again, it’s still too early to say for sure that treating a sleep disorder reduces your risk of dementia because of reduced levels of toxins in the brain.

So where does this leave us?

Collectively, these studies suggest enough good quality sleep is important for a healthy brain, and in particular for clearing toxins associated with dementia from the brain.

But we still don’t know if treating a sleep disorder or improving sleep more broadly affects the brain’s ability to remove toxins, and whether this reduces the risk of dementia. It’s an area researchers, including us, are actively working on.

For instance, we’re investigating the concentration of Aβ and tau measured in blood across the 24-hour sleep-wake cycle in people with sleep apnoea, on and off treatment, to better understand how sleep apnoea affects brain cleaning.

Researchers are also looking into the potential for treating insomnia with a class of drugs known as orexin receptor antagonists to see if this affects the clearance of Aβ from the brain.

If you’re concerned

This is an emerging field and we don’t yet have all the answers about the link between disrupted sleep and dementia, or whether better sleep can boost the glymphatic system and so prevent cognitive decline.

So if you are concerned about your sleep or cognition, please see your doctor.

Julia Chapman, Clinical Trials Lead and Postdoctoral Research Fellow, Woolcock Institute of Medical Research and Conjoint Lecturer, Macquarie University; Camilla Hoyos, Senior Lecturer in the Centre for Sleep and Chronobiology, Macquarie University, and Craig Phillips, Associate Professor, Macquarie Medical School, Macquarie University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Categories : IT in Healthcare NeurologyTags :

Human Instruction with AI Guidance Gives the Best Results in Neurosurgical Training

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Study has implications beyond medical education, suggesting other fields could benefit from AI-enhanced training

Artificial intelligence (AI) is becoming a powerful new tool in training and education, including in the field of neurosurgery. Yet a new study suggests that AI tutoring provides better results when paired with human instruction.

Researchers at the Neurosurgical Simulation and Artificial Intelligence Learning Centre at The Neuro (Montreal Neurological Institute-Hospital) of McGill University are studying how AI and virtual reality (VR) can improve the training and performance of brain surgeons. They simulate brain surgeries using VR, monitor students’ performance using AI and provide continuous verbal feedback on how students can improve performance and prevent errors. Previous research has shown that an intelligent tutoring system powered by AI developed at the Centre outperformed expert human teachers, but these instructors were not provided with trainee AI performance data.

In their most recent study, published in JAMA Surgery, the researchers recruited 87 medical students from four Quebec medical schools and divided them into three groups: one trained with AI-only verbal feedback, one with expert instructor feedback, and one with expert feedback informed by real-time AI performance data. The team recorded the students’ performance, including how well and how quickly their surgical skills improved while undergoing the different types of training.

They found that students receiving AI-augmented, personalised feedback from a human instructor outperformed both other groups in surgical performance and skill transfer. This group also demonstrated significantly better risk management for bleeding and tissue injury – two critical measures of surgical expertise. The study suggests that while intelligent tutoring systems can provide standardised, data-driven assessments, the integration of human expertise enhances engagement and ensures that feedback is contextualised and adaptive.

“Our findings underscore the importance of human input in AI-driven surgical education,” said lead study author Bianca Giglio. “When expert instructors used AI performance data to deliver tailored, real-time feedback, trainees learned faster and transferred their skills more effectively.”

While this study was specific to neurosurgical training, its findings could carry over to other professions where students must acquire highly technical and complex skills in high-pressure environments.

“AI is not replacing educators – it’s empowering them,” added senior author Dr Rolando Del Maestro, a neurosurgeon and current Director of the Centre. “By merging AI’s analytical power with the critical guidance of experienced instructors, we are moving closer to creating the ‘Intelligent Operating Room’ of the future capable of assessing and training learners while minimising errors during human surgical procedures.”

Source: McGill University

Categories : Neurology Obstetrics & GynaecologyTags :

Mother’s Microbes Play Role in Neonatal Brain Development

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Photo by Christian Bowen on Unsplash

New research from Michigan State University finds that microbes play an important role in shaping early brain development, specifically in a key brain region that controls stress, social behaviour, and vital body functions.

The study, published in Hormones and Behavior, used a mouse model to highlight how natural microbial exposure not only impacts brain structure immediately after birth but may even begin influencing development while still in the womb. A mouse model was chosen because mice share significant biological and behavioural similarities with humans and there are no other alternatives to study the role of microbes on brain development.

This work is of significance because modern obstetric practices, like peripartum antibiotic use and Cesarean delivery, disrupt maternal microbes. In the United States alone, 40% of women receive antibiotics around childbirth and one-third of all births occur via Cesarean section.

“At birth, a newborn body is colonised by microbes as it travels through the birth canal. Birth also coincides with important developmental events that shape the brain. We wanted to further explore how the arrival of these microbes may affect brain development,” said Alexandra Castillo Ruiz, lead author of the study and assistant professor in the MSU Department of Psychology.

The research team focused on a brain region called the paraventricular nucleus of the hypothalamus (PVN), which plays a central role in regulating stress, blood pressure, water balance, and even social behaviour. Their previous work had shown that mice raised without microbes, or germ-free mice, had more dying neurons in the PVN during early development. The new study set out to determine whether this increased cell death translated to changes in neuron number in the long run, and if any effects could be caused by the arrival of microbes at birth or if they began in the womb via signals from maternal microbes.

To find out, the researchers used a cross-fostering approach. Germ-free newborn mice were placed with mothers that had microbes and compared them to control groups. When the brains of these mice were examined just three days after birth, results were striking: All mice gestated by germ-free mothers had fewer neurons in the PVN, regardless of whether they received microbes after birth. They also found that germ-free adult mice had fewer neurons in the PVN.

“Our study shows that microbes play an important role in sculpting a brain region that is paramount for body functions and social behaviour. In addition, our study indicates that microbial effects start in the womb via signaling from maternal microbes,” said Castillo-Ruiz.

Rather than shunning our microbes, we should recognise them as partners in early life development,” said Castillo-Ruiz. “They’re helping build our brains from the very beginning.”

Source: Michigan State University