Category: Neurology

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

Categories : Lab Tests and Imaging NeurologyTags :

Test Detects Brain Cancers in Cerebrospinal Fluid with High Accuracy

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Photo by Cottonbro on Pexels

A novel, multi-analyte test developed by researchers at Johns Hopkins Medicine can accurately identify brain cancers using small samples of cerebrospinal fluid (CSF), offering a promising new tool to guide clinical decision-making.

The findings, supported by funding from the National Institutes of Health, were published in Cancer Discovery and demonstrate that combining multiple biological markers, including tumour-derived DNA and immune cell signatures, is more effective for diagnosing central nervous system cancers than using any one marker alone.

“This study highlights how much more information we can gain when we evaluate several analytes together,” says senior study author Chetan Bettegowda, MD, PhD, Professor and Director of the Department of Neurosurgery at the Johns Hopkins University School of Medicine. “The ability to detect cancers with high specificity and also gain insight into the immune environment of the brain could be an important advance in the care of patients with brain tumours.”

To evaluate the potential of a multi-analyte approach, investigators analysed 206 CSF samples, including samples from patients with high-grade gliomas, medulloblastomas, metastases and central nervous system lymphomas. Their test, called CSF-BAM (cerebrospinal fluid–B/T cell receptor, aneuploidy and mutation), measured chromosomal abnormalities, tumour-specific mutations, and T and B cell receptor sequences. In combination, these markers identified brain cancers with more than 80% sensitivity (ability to detect cancer) and 100% specificity (correctly identified those who were cancer-free) in the validation cohort. The 100% specificity means no false positives were recorded among individuals with noncancerous conditions.

The study also showed that the assay could distinguish between the immune cell populations present in cancer and noncancer cases, offering additional biological context that could be helpful in more-challenging clinical scenarios. Investigators say this ability to categorize T and B cell populations in the CSF provides insights into both disease presence and immune response.

“Many patients with brain lesions face invasive diagnostic procedures to confirm a cancer diagnosis,” says Christopher Douville, MD, assistant professor of oncology and a senior study author. “A tool like this could help us make better-informed decisions about who really needs a biopsy and who doesn’t.”

Researchers say the test could be particularly useful for cases in which conventional imaging or cytology is inconclusive, or in situations when obtaining tissue for diagnosis is risky or not possible. The multi-analyte approach, they say, enables clinicians to better detect cancer and better understand the disease status, supporting a more tailored approach to patient care.

Source: Johns Hopkins Medicine

Categories : Neurology Regenerative MedicineTags : 1 Comment

Groundbreaking Spinal Scaffold Allows Nerve Fibres to Regrow

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New research combines 3D printing, stem cell biology, and lab-grown tissues for possible treatments of spinal cord injuries. Photo provided by: McAlpine Research Group, University of Minnesota

For the first time, a research team at the University of Minnesota Twin Cities demonstrated a groundbreaking process that combines 3D printing, stem cell biology, and lab-grown tissues for spinal cord injury recovery. 

The study was recently published in Advanced Healthcare Materials. Currently, there is no way to completely reverse the damage and paralysis from the injury. A major challenge is the death of nerve cells and the inability of nerve fibres to regrow across the injury site. This new research tackles this problem head-on.

The method involves creating a unique 3D-printed framework for lab-grown organs, called an organoid scaffold, with microscopic channels. These channels are then populated with regionally specific spinal neural progenitor cells (sNPCs), which are cells derived from human adult stem cells that have the capacity to divide and differentiate into specific types of mature cells.

“We use the 3D printed channels of the scaffold to direct the growth of the stem cells, which ensures the new nerve fibres grow in the desired way,” said Guebum Han, a former University of Minnesota mechanical engineering postdoctoral researcher and first author on the paper who currently works at Intel Corporation. “This method creates a relay system that when placed in the spinal cord bypasses the damaged area.”

n their study, the researchers transplanted these scaffolds into rats with spinal cords that were completely severed. The cells successfully differentiated into neurons and extended their nerve fibres in both directions – rostral (toward the head) and caudal (toward the tail) – to form new connections with the host’s existing nerve circuits. 

The new nerve cells integrated seamlessly into the host spinal cord tissue over time, leading to significant functional recovery in the rats.

“Regenerative medicine has brought about a new era in spinal cord injury research,” said Ann Parr, professor of neurosurgery at the University of Minnesota. “Our laboratory is excited to explore the future potential of our ‘mini spinal cords’ for clinical translation.”

While the research is in its beginning stages, it offers a new avenue of hope for those with spinal cord injuries. The team hopes to scale up production and continue developing this combination of technologies for future clinical applications.

Source: University of Minnesota

Categories : Metabolic Disorders NeurologyTags :

New Research Shows that Macrophages Help Prevent the Development of Neuropathy

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Source: Pixabay CC0

An increase in high-fat, high-fructose foods in people’s diets has contributed to a dramatic increase in type 2 diabetes. This, in turn, has led to an increase in peripheral neuropathy. About half of people with type 2 diabetes are affected, and of these, about half experience severe neuropathic pain.

The damage begins as axons from sensory neurons begin to retract and disappear from the tissues they innervate. New research from the lab of Clifford Woolf, MB, BCh, PhD, director of the F.M. Kirby Neurobiology Center at Boston Children’s Hospital, reveals that months before the damage occurs, immune cells flood into peripheral nerves in an apparent attempt to protect them. This surprising insight, published in Nature, could lead to strategies to prevent peripheral neuropathy or at least minimize and slow the onset of the damage.

Immune cells prevent nerve damage

A team led by Sara Hakim, PhD, a graduate student in the lab, created a mouse model of diabetes induced by a high-fat, high-fructose diet. The model showed that these mice developed all the major features of diabetes within eight to 12 weeks of starting the diet. At about six months, axons in the skin began to degenerate, indicating the presence of neuropathy.

“Diabetic neuropathy takes years, or even decades to develop in humans,” says Hakim, who is now at Vertex. “By using a mouse model in which symptoms slowly develop over months, we were able to catch the progression of the disease over time, and observe those early protective responses when the body is still trying to fight the disease.”

The researchers suspected that peripheral neuropathy is caused by the immune system, so used single-cell sequencing to detect changes in immune cells near sensory neuron axons in peripheral nerves.

One type of immune cell residing in nerves, a pro-inflammatory macrophage, began producing chemokines. These signaling molecules recruited a second population of circulating macrophages, which began infiltrating the nerve 12 weeks after the mice began the diet – as sensory symptoms were starting to appear but before nerve degeneration was seen.

Previously, macrophages were thought to have a pathogenic role in diabetes and were mainly reacting to axon loss. But Hakim, Woolf, and colleagues observed just the opposite.

“To our great surprise, when we blocked infiltration of macrophages into the nerve, neuropathy started getting worse, not better,” says Woolf. “The macrophages were protective. They slowed down the onset of neuropathy and reduced its impact.”

Potential strategies for peripheral neuropathy

The Woolf Lab is now exploring how the infiltrating macrophages protect against peripheral neuropathy. The next step would be to find a way to induce and sustain this protection and identify biomarkers that would flag those people with diabetes who are at risk.

One potential protective strategy might involve accelerating the recruitment of macrophages into nerves; another might involve mimicking their protective function by harnessing compounds they secrete, such as galectin 3.

“Since we could profile the cells and identify what genes they are expressing, we found a number of signalling molecules known to be protective,” says Woolf. “We can now go through that list and check to see which are most active.”

The latest work reinforces the idea that pain isn’t just a disease of neurons, but results from interactions between the nervous system and the immune system. In a study last year, the Woolf Lab discovered thousands of molecular interactions between pain-sensing neurons and different types of immune cells.

Now, the plot is thickening with this example of immune cells acting to prevent painful nerve damage. “We’ve now revealed a novel, slower protective effect of the immune system,” Woolf says.

Source: Boston Children’s Hospital

Categories : Cancer NeurologyTags :

Researchers Find TBI Link to Development of Malignant Brain Tumours

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

New research led by investigators at Mass General Brigham suggests a link between a history of traumatic brain injury (TBI) and risk of developing a malignant brain tumour. By evaluating data from 2000–2024 of more than 75 000 people with a history of mild, moderate or severe TBI, the team found the risk of developing a malignant brain tumour was significantly higher compared to people without a history of TBI. The results were published in JAMA Network Open.

“I see these results as alarming,” said co-senior author and corresponding author Saef Izzy, MD, FNCS, FAAN, a neurologist and head of the Immunology of CNS Injury Program at Brigham and Women’s Hospital, a founding member of the Mass General Brigham healthcare system. “Our work over the past five years has shown that TBI is a chronic condition with lasting effects. Now, evidence of a potential increased risk of malignant brain tumours adds urgency to shift the focus from short-term recovery to lifelong vigilance.

“Alongside our earlier findings linking TBI and cardiovascular disease, this underscores the importance of long-term monitoring for anyone with a history of TBI.”

The team divided the severity of TBI between mild, moderate and severe, with participants suffering from incidents ranging from car accidents to falls. In the two categories of moderate and severe, 0.6% of people (87 out of 14 944) developed brain tumours within 3-to-5 years after the TBI, which was a higher percentage than controls. Mild cases of TBI, such as those caused by concussions, were not associated with an increased risk of tumour. The aim of the study was not to establish a cause-and-effect link between moderate-to-severe TBI and malignant tumours, but rather to explore whether an association exists. Determining causality and understanding the underlying mechanisms will require a dedicated translational study in the future.

A previous study showed veterans of the Iraq and Afghanistan wars who suffered TBI experienced an increased risk of brain tumours, but previous studies on civilian populations showed conflicting results. The collaborative team of researchers used an international disease classifying system known as ICD codes to exclude anyone in the study with a history of brain tumour, benign tumours, and risk factors such as radiation exposure.

Previous neurotrauma studies from Mass General Brigham have looked at patients with a history of TBI and found an association with the emergence of anxiety, depression, and other psychiatric, neurological, and cardiovascular diseases, but the current study focuses on malignant tumour development.

Future imaging studies could draw a connection between the location of the TBI and where tumours developed in the brains of participants. The team would like to further study patients with repeated injuries, such as falls. 

“While there is an increased risk of tumour from TBI, the overall risk remains low. Still, brain tumour is a devastating disease and often gets detected in later stages,” said lead author Sandro Marini, MD, a neurologist at Mass General Brigham. “Now, we’ve opened the door to monitor TBI patients more closely.”

Source: Mass General Brigham