Category: Neurology

Categories : NeurologyTags :

Scientists Uncover the Brain Mechanisms that Distinguish Imagination from Reality

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Areas of the brain that help a person differentiate between what is real and what is imaginary have been uncovered in a new study led by UCL researchers. The research, published in Neuron, found that a region in the brain known as the fusiform gyrus – located behind one’s temples, on the underside of the brain’s temporal lobe – is involved in helping the brain to determine whether what we see is from the external world or generated by our imagination.

The researchers hope that their findings will increase understanding of the cognitive processes that go awry when someone has difficulty judging what is real and what is not, such as in schizophrenia, and could eventually lead to advancement in diagnosing and treating these conditions.

Lead author, Dr Nadine Dijkstra (Department of Imaging Neuroscience at UCL) said: “Imagine an apple in your mind’s eye as vividly as you can. During imagination, many of the same brain regions activate in the same manner as when you see a real apple. Until recently, it remained unclear how the brain distinguishes between these real and imagined experiences.”

For the study, researchers asked 26 participants to look at simple visual patterns while imagining them at the same time.

Specifically, participants were asked to look for a specific faint pattern within a noisy background on a screen and indicate whether the pattern was actually present or not. A real pattern was only presented half of the time.

At the same time, participants were also instructed to imagine a pattern that was either the same or different to the one they were looking for, and indicate how vivid their mental images were.

When the patterns were the same, and participants reported that their imagination was very vivid, they were more likely to say they saw a real pattern, even on trials in which nothing was presented. This means they mistook their mental images for reality.

While participants performed the tasks, their brain activity was monitored using functional magnetic resonance imaging (fMRI). This technology enabled the researchers to identify which parts of the brain showed patterns of activity that helped distinguish reality from imagination.

The team found that the strength of activity in the fusiform gyrus could predict whether people judged an experience as real or imagined, irrespective of whether it actually was real.

When activity in the fusiform gyrus was strong, people were more likely to indicate that the pattern was really there.

Usually, activation in the fusiform gyrus is weaker during imagination than during perception, which helps the brain keep the two apart. However, this study showed that sometimes when participants imagined very vividly, activation of the fusiform gyrus was very strong and participants confused their imagination for reality.

Senior author, Professor Steve Fleming (UCL Psychology & Language Sciences) said: “The brain activity in this area of visual cortex matched the predictions from a computer simulation on how the difference between internally and externally generated experience is determined.”

Dr Dijkstra added: “Our findings suggest that the brain uses the strength of sensory signals to distinguish between imagination and reality.”

The study also showed that the fusiform gyrus collaborates with other brain areas to help us decide what is real and what is imagined.

Specifically, activity in the anterior insula – a brain region in the prefrontal cortex (the front part of the brain that acts as a control centre for tasks such as decision making, problem solving and planning) – increased in line with activity in the fusiform gyrus when participants said something was real, even if it was in fact imagined.

Professor Fleming said: “These areas of the prefrontal cortex have previously been implicated in metacognition – the ability to think about our own minds. Our results indicate that the same brain areas are also involved in deciding what is real.”

These results offer new insights into what might go wrong in the brain during psychiatric conditions like schizophrenia where patients struggle keeping apart imagination and reality. The findings may also inform future virtual reality technologies by identifying how and when imagined experiences feel real.

Source: University College London

Categories : NeurologyTags :

Dancing Brainwaves – How Sound Reshapes Brain Networks in Real Time

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Photo by jonas mohamadi

Every beep,  tone and new sound you hear travels from the ear to registering in your brain. But what actually happens in your brain when you listen to a continuous stream of sounds? A new study from Aarhus University and University of Oxford published in Advanced Science reveals that the brain doesn’t simply register sound: it dynamically reshapes its organisation in real time, orchestrating a complex interplay of brainwaves in multiple networks.

The research, led by Dr Mattia Rosso and Associate Professor Leonardo Bonetti at the Center for Music in the Brain, Aarhus University, in collaboration with the University of Oxford, introduces a novel neuroimaging method called  FREQ-NESS – Frequency-resolved Network Estimation via Source Separation. Using advanced algorithms, this method disentangles overlapping brain networks based on their dominant frequency. Once a network is identified by its unique frequency, the method can then trace how it propagates in space across the brain.

“We’re used to thinking of brainwaves like fixed stations – alpha, beta, gamma – and of brain anatomy as a set of distinct regions”, says Dr Rosso. “But what we see with FREQ-NESS is much richer. It is long known that brain activity is organised through activity in different frequencies, tuned both internally and to the environment. Starting from this fundamental principle, we’ve designed a method that finds how each frequency is expressed across the brain.”

Opens the door to precise brain mapping

The development of FREQ-NESS represents a major advance in how scientists can investigate the brain’s large-scale dynamics. Unlike traditional methods that rely on predefined frequency bands or regions of interest, the data-driven approach maps the whole brain’s internal organisation with high  spectral and spatial precision. And that opens new possibilities for basic neuroscience, brain-computer interfaces, and clinical diagnostics.

This study adds to a growing body of research exploring how the brain’s rhythmic structure shapes everything from music cognition to general perception and attention, and altered states of consciousness.

“The brain doesn’t just react: it reconfigures. And now we can see it”, says Professor Leonardo Bonetti, co-author and neuroscientist at Center for Music in the Brain, Aarhus University, and at the Centre for Eudaimonia and Human Flourishing, University of Oxford. “This could change how we study brain responses to music and beyond, including consciousness, mind-wandering, and broader interactions with the external world.”

A large-scale research program is now underway to build on this methodology, supported by an international network of neuroscientists. Due to the high reliability across experimental conditions and across datasets – FREQ-NESS might also pave the way for individualised brain mapping, explains Professor Leonardo Bonetti.

Source: Aarhus University

Categories : NeurologyTags :

Hormone Supplementation in Rhesus Monkeys Points to Potential Autism Treatment

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For years, Florida Tech’s Catherine Talbot, assistant professor of psychology, has worked to understand the sociality of male rhesus monkeys and how low-social monkeys can serve as a model for humans with autism. Her most recent findings show that replenishing a deficient hormone, vasopressin, helped the monkeys become more social without increasing their aggression – a discovery that could change autism treatment.

Currently, the Centers for Disease Control and Prevention report that one in 36 children in the United States is affected by autism spectrum disorder (ASD). That’s an increase from one in 44 children reported in 2018. Two FDA-approved treatments currently exist, Talbot said, but they only address associated symptoms, not the root of ASD. The boost in both prevalence and awareness of the disorder prompts the following question: What is the cause?

Some rhesus monkeys are naturally low-social, meaning they demonstrate poor social cognitive skills, while others are highly social. Their individual variation in sociality is comparable to how human sociality varies, ranging from people we consider social butterflies to those who are not interested in social interactions, similar to some people diagnosed with ASD, Talbot said. Her goal has been to understand how variations in biology and behaviour influence social cognition.

In their paper published in the journal PNAS, Talbot and researchers with Stanford, the University of California, Davis and the California National Primate Research Center explored vasopressin, a hormone that is known to contribute to mammalian social behaviour, as a potential therapeutic treatment that may ultimately help people with autism better function in society. Previous work from this research group found that vasopressin levels are lower in their low-social rhesus monkey model, as well as in a select group of people with ASD.

Previous studies testing vasopressin in rodents found that increased hormone levels caused more aggression. As a result, researchers warned against administering vasopressin as treatment, Talbot said. However, she argued that in those studies, vasopressin induced aggression in contexts where aggression is the socially appropriate response, such as guarding mates in their home territory, so the hormone may promote species-typical behaviour.

She also noted that the previous studies tested vasopressin in “neurotypical” rodents, as opposed to animals with low-social tendencies.

“It may be that individuals with the lowest levels of vasopressin may benefit the most from it – that is the step forward toward precision medicine that we now need to study,” Talbot said.

In her latest paper, Talbot and her co-authors tested how low-social monkeys, with low vasopressin levels and high autistic-like trait burden, responded to vasopressin supplementation to make up for their natural deficiency. They administered the hormone through a nebulizer, which the monkeys could opt into. For a few minutes each week, the monkeys voluntarily held their face up to a nebulizer to receive their dose while sipping white grape juice – a favorite among the monkeys, Talbot said.

After administering the hormone and verifying that it increased vasopressin levels in the central nervous system, the researchers wanted to see how the monkeys responded to both affiliative and aggressive stimuli by showing them videos depicting these behaviors. They also compared their ability to recognize and remember new objects and faces, which is another important social skill.

They found that normally low-social monkeys do not respond to social communication and were better at recognizing and remembering objects compared to faces, similar to some humans diagnosed with ASD. When the monkeys were given vasopressin, they began reciprocating affiliative, pro-social behaviors, but not aggression. It also improved their facial recognition memory, making it equivalent to their recognition memory of objects.

In other words, vasopressin “rescued” low-social monkeys’ ability to respond prosocially to others and to remember new faces. The treatment was successful – vasopressin selectively improved the social cognition of these low-social monkeys.

“It was really exciting to see this come to fruition after pouring so much work into this project and overcoming so many challenges,” Talbot said of her findings.

One of Talbot’s co-authors has already begun translating this work to cohorts of autism patients. She expects more clinical trials to follow.

In the immediate future, Talbot is examining how other, more complex social cognitive abilities like theory of mind – the ability to take the perspective of another – may differ in low-social monkeys compared to more social monkeys and how this relates to their underlying biology. Beyond that, Talbot hopes that they can target young monkeys who are “at-risk” of developing social deficits related to autism for vasopressin treatment to see if early intervention might help change their developmental trajectory and eventually translate this therapy to targeted human trials. 

Source: Florida Tech

Categories : Neurology UrogenitalTags :

Brain Stimulation and Mindfulness Exercises Could Reduce ‘Latchkey Incontinence’

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Urinary incontinence. Credit: Scientific Animations CC4.0

Arriving home after a long day may be a relief, but for some people, seeing their front door or inserting a key into the lock triggers a powerful urge to pee. Known as “latchkey incontinence,” this phenomenon is the subject of a new study by researchers at the University of Pittsburgh who found that mindfulness training and/or non-invasive brain stimulation could reduce bladder leaks and feelings of urgency evoked by these cues. 

The findings of the pilot study, the first evaluation of brain-based therapies for urinary incontinence, are published in the latest issue of the journal Continence. 

“Incontinence is a massive deal,” said senior author Dr. Becky Clarkson, research assistant professor in the Pitt School of Medicine Division of Geriatrics and co-director of the Continence Research Center. “Bladder leaks can be really traumatizing. People often feel like they can’t go out and socialise or exercise because they’re worried about having an accident. Especially for older adults, this feeds into social isolation, depression and functional decline. Our research aims to empower people with tools to get back their quality of life.” 

Latchkey incontinence, or situational urgency urinary incontinence, is bladder leakage triggered by specific environments or scenarios. Common cues include one’s front or garage door, running water, getting into a car or walking past public restrooms. 

According to lead author Dr. Cynthia Conklin, associate professor in the Pitt Department of Psychiatry, latchkey incontinence is a type of Pavlovian conditioning. Like Pavlov’s dogs, which salivated upon hearing a bell that they associated with food, years of going to the bathroom immediately upon entering the house can condition one to feel strong bladder urgency when seeing the front door.

In a previous study, Clarkson and Conklin showed participants pictures of their own front doors or other triggers versus “safe” images of things that did not evoke urgency while they had an MRI of their brain. A part of the brain called the dorsolateral prefrontal cortex was more active when participants viewed urgency-related images.  

“The prefrontal cortex is the seat of cognitive control,” said Clarkson. “It’s the executive function center of the bladder, the bit that is telling you, ‘Okay, it’s time to go. You should find somewhere to go.’” 

The researchers hypothesised that activating this part of the brain during exposure to urgency cues, through mindfulness and/or with transcranial direct current stimulation (tDCS) of the brain, could improve participants’ ability to regulate responses to these cues and control urgency and leakage.  

They recruited 61 women aged over 40 who reported regular situationally triggered bladder leaks and randomly assigned them to one of three groups: Participants either listened to a 20-minute mindfulness exercise, received tDCS or both while viewing personal trigger photos.  

The mindfulness exercise, developed by coauthor Dr Carol Greco, associate professor of psychiatry and physical therapy at Pitt, was like a typical body scan practice that instructs participants to move through their body, bringing attention to each part in turn. But unlike most body scans, it included specific acknowledgment of bladder sensation.  

After completing four in-office sessions over five to six days, participants in all three groups experienced reduced urgency when they viewed trigger cues. Women in all three groups also reported an improvement in the number of urgency episodes and leaks after completing the sessions. 

Although this pilot study did not have a control group, for comparison, the researchers say that the magnitude of improvement from tDCS and mindfulness was similar to what other research has reported for interventions such as medications and pelvic floor therapy.  

“Although we need to do more research, these results are really encouraging because they suggest that a behavioral tool like mindfulness can be an alternative or additional way to improve symptoms,” said Conklin. “Balancing multiple prescriptions is a big issue among older adults, and a lot of people are reluctant to take another medication, so I think that’s one of the reasons that we saw such high acceptability of non-pharmacologic interventions in this study.” 

More than 90% of recruited participants completed the study.  

“Participants loved it,” said Clarkson. “Almost everyone who started the study finished it, even though coming into the office four days within one week was quite a big commitment. We got really great feedback, and a lot of women told us that they continue to use the mindfulness exercise in their daily lives.” 

“For the first time in 20 years of doing research, we got thank you cards!” added Conklin. “I think that incontinence is such a taboo subject, and a lot of people find it difficult to talk about, so they often don’t even realize that there are treatments out there. But you don’t have to suffer in silence.” 

Now, the researchers are planning to explore whether the mindfulness component of the study could be helpful in independent living facilities to reach a wide range of older adults. They also hope to eventually develop an app-based tool for smartphones. 

Source: University of Pittsburgh

Categories : Diet and Nutrition NeurologyTags :

What Does Caffeine Do to the Sleeping Brain?

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Caffeine is one of the most widely consumed psychoactive substances in the world, present in tea, coffee, chocolate and energy drinks. In a study published in Nature Communications Biology, a team of researchers from Université de Montréal shed new light on how caffeine can modify sleep and influence the brain’s recovery, both physical and cognitive, overnight.

The research was led by Philipp Thölke, a research trainee at UdeM’s Cognitive and Computational Neuroscience Laboratory (CoCo Lab), and co-led by the lab’s director Karim Jerbi, a psychology professor and researcher at Mila – Quebec AI Institute.

Working with sleep-and-aging psychology professor Julie Carrier and her team at UdeM’s Centre for Advanced Research in Sleep Medicine, the scientists used AI and electroencephalography (EEG) to study caffeine’s effect on sleep.

They showed for the first time that caffeine increases the complexity of brain signals and enhances brain “criticality” during sleep.  Interestingly, this was more pronounced in younger adults.

“Criticality describes a state of the brain that is balanced between order and chaos,” said Jerbi.

“It’s like an orchestra: too quiet and nothing happens, too chaotic and there’s cacophony. Criticality is the happy medium where brain activity is both organised and flexible. In this state, the brain functions optimally: it can process information efficiently, adapt quickly, learn and make decisions with agility.”

Added Carrier: “Caffeine stimulates the brain and pushes it into a state of criticality, where it is more awake, alert and reactive. While this is useful during the day for concentration, this state could interfere with rest at night: the brain would neither relax nor recover properly.”

Nocturnal brain activity

To study how caffeine affects the sleeping brain, Carrier’s team recorded the nocturnal brain activity of 40 healthy adults using an electroencephalogram.  They compared each participant’s brain activity on two separate nights, one when they consumed caffeine capsules three hours and then one hour before bedtime, and another when they took a placebo at the same times.

“We used advanced statistical analysis and artificial intelligence to identify subtle changes in neuronal activity,” said Thölke, the study’s first author. “The results showed that caffeine increased the complexity of brain signals, reflecting more dynamic and less predictable neuronal activity, especially during the non-rapid eye movement (NREM) phase of sleep that’s crucial for memory consolidation and cognitive recovery.”

The researchers also discovered striking changes in the brain’s electrical rhythms during sleep: caffeine attenuated slower oscillations such as theta and alpha waves (generally associated with deep, restorative sleep) and stimulated beta wave activity, which is more common during wakefulness and mental engagement.

“These changes suggest that even during sleep, the brain remains in a more activated, less restorative state under the influence of caffeine,” says Jerbi, who also holds the Canada Research Chair in Computational Neuroscience and Cognitive Neuroimaging. “This change in the brain’s rhythmic activity may help explain why caffeine affects the efficiency with which the brain recovers during the night, with potential consequences for memory processing.”

People in their 20s more affected

The study also showed that the effects of caffeine on brain dynamics were significantly more pronounced in young adults between ages 20 and 27 compared to middle-aged participants aged 41 to 58, especially during REM sleep, the phase associated with dreaming.

Young adults showed a greater response to caffeine, likely due to a higher density of adenosine receptors in their brains. Adenosine is a molecule that gradually accumulates in the brain throughout the day, causing a feeling of fatigue.

“Adenosine receptors naturally decrease with age, reducing caffeine’s ability to block them and improve brain complexity, which may partly explain the reduced effect of caffeine observed in middle-aged participants,” Carrier said.

And these age-related differences suggest that younger brains may be more susceptible to the stimulant effects of caffeine. Given caffeine’s widespread use, the researchers stress the importance of understanding its complex effects on brain activity across different age groups and health conditions.

They add that further research is needed to clarify how these neural changes affect cognitive health and daily functioning, and to potentially guide personalised recommendations for caffeine intake.

Source: University of Montreal

Categories : Neurodegenerative Diseases NeurologyTags :

Autism Linked to Elevated Risk of Parkinson’s Disease

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People with an autism diagnosis are at a higher risk of developing Parkinson’s disease early in life, according to a large-scale study from Karolinska Institutet. The researchers believe that the two conditions can share underlying biological mechanisms.

The study, published in JAMA Neurology, is based on registry data from over two million people born in Sweden between 1974 and 1999 who were followed from the age of 20 up to the end of 2022.

The researchers interrogated a possible connection between the neuropsychiatric diagnosis Autism Spectrum Disorder (ASD), which affects an individual’s thought processes, behaviour and interpersonal communication, and early-onset Parkinson’s disease, a condition that affects locomotion and movement.

Possible dopamine involvment

The results show that people with an autism diagnosis were four times more likely to develop Parkinson’s disease than people without such a diagnosis, a correlation that remained when controlling for socioeconomic status, a genetic predisposition for mental illness or Parkinson’s disease and other such factors.

“This indicates that there can be shared biological drivers behind ASD and Parkinson’s disease,” says first author Weiyao Yin at the Department of Medical Epidemiology and Biostatistics. “One hypothesis is that the brain’s dopamine system is affected in both cases, since the neurotransmitter dopamine plays an important part in social behaviour and motion control.”

It is well-known that dopamine-producing neurons are degraded in Parkinson’s disease. Previous studies have also shown that dopamine is possibly implicated in autism, but more research needs to be done to confirm this.

“We hope that our results will eventually help to bring greater clarity to the underlying causes of both ASD and Parkinson’s disease,” says Dr Yin.

Medical checkups are vital

Depression and the use of antidepressants are common in people with autism, as are antipsychotic drugs, which are known for being able to cause Parkinson’s-like symptoms. When the researchers adjusted for these factors, the correlation between ASD and the later development of Parkinson’s disease was less salient, but the risk was still double.

The researchers point out that they only analysed early-onset Parkinson’s disease before the age of 50 and that the average age of participants by the end of the study was 34. The incidence of Parkinson’s disease was therefore very low. Future studies will need to examine if the elevated risk persists into older age. 

“The healthcare services need to keep people with ASD – a vulnerable group with high co-morbidity and a high use of psychotropics – under long-term observation,” says last author Sven Sandin, statistician and epidemiologist at the Department of Medical Epidemiology and Biostatistics. “At the same time, it’s important to remember that a Parkinson’s diagnosis before the age of 50 is very rare, including for people with autism.”

Source: Karolinska Institutet

Categories : NeurologyTags :

How Molecules can ‘Remember’ and Contribute to Memory and Learning

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Source: CC0

Researchers have discovered how an ion channel in the brain’s neurons has a kind of ‘molecular memory’, which contributes to the formation and preservation of lifelong memories. The researchers have identified a specific part of the ion channel at which new drugs for certain genetic diseases could be targeted.

Learning from past experiences and forming memories depend on the reshaping of connections between neurons in the brain. Synapses are strengthened or weakened throughout life in such a way that the brain is, in a certain sense, constantly being reshaped at the cellular level. This phenomenon is called synaptic plasticity.

There are several processes contributing to synaptic plasticity in the nervous system. One of these processes has to do with a type of molecules called calcium ion channels, which have long been of interest to researchers at Linköping University, LiU.

“I want to uncover the secret lives of these ion channel molecules. Calcium ion channels have very important functions in the body – by opening and closing, they regulate, among other things, nerve-to-nerve signalling. But beyond that, these molecules also have a kind of memory of their own, and can remember previous nerve signals,” says Antonios Pantazis, associate professor at the Department of Biomedical and Clinical Sciences at LiU, who led the study published in Nature Communications.

How can a molecule remember?

The focus of this study was on a specific type of ion channel, the CaV2.1 channel, which is the most common calcium ion channel in the brain. The ion channel is located at the synapse, at the very end of the neuron. When an electrical signal passes through the neuron, the ion channel open, setting in motion a process leading to neurotransmitter being released towards the receiving neuron in the synapse. In this way, CaV2.1 channels are the gatekeepers of synaptic, neuron-to-neuron communication.

Prolonged electrical activity reduces the number of CaV2.1 channels that can open, resulting in less transmitter release, so the receiving neuron receives a weaker message. It is as if the channels can ‘remember’ previous signalling, and in doing so, make themselves unavailable to open by subsequent signals. How this works at the molecular level has been unknown to scientists until now.

The Linköping researchers have now discovered a mechanism for how the ion channel can ‘remember’. The channel is a large molecule made up of several interconnected parts, which can move relative to each other in response to electrical signals. They discovered that the ion channel can take almost 200 different shapes depending on the strength and duration of an electrical signal; it is a very complex molecular machine.

“We believe that during sustained electrical nerve signalling, an important part of the molecule disconnects from the channel gate, similar to the way the clutch in a car breaks the connection between the engine and the wheels. The ion channel can then no longer be opened. When hundreds of signals occur over long enough time, they can convert most channels into this ‘declutched memory state’ for several seconds,” says Antonios Pantazis.

Target for future drugs

If the ion channel can ‘remember’ for just a few seconds, how does it contribute to lifelong learning? This type of collective memory in the ion channels can accumulate over time and reduce the communication between two neurons. This then leads to changes in the receiving neuron, lasting for hours or days. Eventually, it results in much longer-lived changes in the brain, such as the elimination of weakened synapses.

“In this way, a ‘memory’ that lasts for a few seconds in a single molecule can make a small contribution to a person’s memory that lasts for a lifetime,” says Antonios Pantazis.

Increased knowledge of how these calcium ion channels work can in the long term contribute to the treatment of certain diseases. There are many variants of the gene that produces the CaV2.1 channel, CACNA1A, that are linked to rare but serious neurological diseases, that often run in families. To develop drugs against these, it helps to know which part of the large ion channel you want to affect and in what way its activity should be changed.

“Our work pinpoints which part of the protein should be targeted when developing new drugs,” says Antonios Pantazis.

Source: Linköping University

Categories : Mental Health NeurologyTags :

Extending Ketamine’s Relieving Effect on Depression

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For 30% of people with major depressive disorder (MDD), antidepressants don’t work. When infused at a low dose, ketamine shows remarkable efficacy as a rapidly acting antidepressant, with effects observed within hours even in patients who have been resistant to other antidepressant treatments. One drawback is that consistent infusions of ketamine are needed to maintain symptoms at bay, which could result in side effects, such as dissociative behaviours and the possibility of addiction, and stopping treatment can result in relapse.

In a new study published in Science, Lisa Monteggia’s and Ege Kavalali’s labs show that it is feasible to substantially extend the efficacy of a single dose of ketamine from its current duration of up to a week to a longer period of up to two months.

“The premise of this study, which was led by Zhenzhong Ma, a fantastic research assistant professor, was based on a testable mechanistic model that we developed that accounts for ketamine’s rapid antidepressant action,” Monteggia said.

Previously, researchers in the field had determined that ketamine’s antidepressant effect requires the activation of a key signalling pathway called ERK, but only ketamine’s long-term effects – not its rapid effects – are abolished when ERK is inhibited. As a fast-acting antidepressant, ketamine relies on ERK-dependent synaptic plasticity to produce its rapid behavioural effects. Ma and colleagues hypothesised that they could maintain ketamine’s effects for longer periods by enhancing ERK activity. 

In the recent paper, Ma discovered that ketamine’s antidepressant effects could be sustained for up to two months by using a drug called BCI, which inhibits a protein phosphatase and results in increased ERK activity. By inhibiting the phosphatase, the authors retained ERK’s activity and augmented the synaptic plasticity that drives ketamine’s prolonged antidepressant effects. 

lthough the use of BCI makes the application of these results to the clinic difficult, Monteggia said that the results provide a proof of principle that ketamine’s antidepressant action can be sustained by targeting intracellular signaling. She and Kavalali, the William Stokes Professor of Experimental Therapeutics and the chair of the Department of Pharmacology, have worked on the project since its inception and hope that it will foster other studies looking to identify specific molecules to enhance and sustain the action of a single dose of ketamine.

Ultimately, this work will be a stepping stone toward improving MDD patients’ lives by reducing the burden of treatment.

Source: Vanderbilt University

Categories : Injury & Trauma NeurologyTags :

Glasgow Coma Scale Joined by New Measures to Assess TBI

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Trauma centres in the United States will begin to test a new approach for assessing traumatic brain injury (TBI) that is expected to lead to more accurate diagnoses and more appropriate treatment and follow-up for patients.

The new framework, which was developed by a coalition of experts and patients from 14 countries and spearheaded by the National Institutes of Health (NIH), expands the assessment beyond immediate clinical symptoms. Added criteria would include biomarkers, CT and MRI scans, and factors such as other medical conditions and how the trauma occurred.

The framework appears in the May 20 issue of Lancet Neurology.

For 51 years, trauma centres have used the Glasgow Coma Scale to assess patients with TBI, roughly dividing them into mild, moderate, and severe categories, based solely on their level of consciousness and a handful of other clinical symptoms.

That diagnosis determined the level of care patients received in the emergency department and afterward. For severe cases, it also influenced the guidance doctors gave the patients’ families, including recommendations around the removal of life support. Yet, doctors have long understood that those tests did not tell the whole story.

“There are patients diagnosed with concussion whose symptoms are dismissed and receive no follow-up because it’s ‘only’ concussion, and they go on to live with debilitating symptoms that destroy their quality of life,” said corresponding author Geoffrey Manley, MD, PhD, professor of neurosurgery at UC San Francisco and a member of the UCSF Weill Institute for Neurosciences. “On the other hand, there are patients diagnosed with ‘severe TBI’ who were eventually able to live full lives after their families were asked to consider removing life-sustaining treatment.”

In the US, TBI resulted in approximately 70 000 deaths in 2021 and accounts for about half-a-million permanent disabilities each year. Motor vehicle accidents, falls, and assault are the most common causes.

New system will better match patients to treatments

Known as CBI-M, the framework comprises four pillars – clinical, biomarker, imaging, and modifiers – that were developed by working groups of federal partners, TBI experts, scientists, and patients.

“The proposed framework marks a major step forward,” said co-senior author Michael McCrea, PhD, professor of neurosurgery and co-director of the Center for Neurotrauma Research at the Medical College of Wisconsin in Milwaukee. “We will be much better equipped to match patients to treatments that give them the best chance of survival, recovery, and return to normal life function.”

The framework was led by the NIH National Institute of Neurological Disorders and Stroke (NIH-NINDS), for which Manley, McCrea, and their co-first and co-senior authors are members of the steering committee on improving TBI characterisation.

The clinical pillar retains the Glasgow Coma Scale’s total score as a central element of the assessment, measuring consciousness and pupil reactivity as an indication of brain function. The framework recommends including the scale’s responses to eye, verbal, and motor commands or stimuli, presence of amnesia, and symptoms like headache, dizziness, and noise sensitivity.

“This pillar should be assessed as first priority in all patients,” said co-senior author Andrew Maas, MD, PhD, emeritus professor of neurosurgery at the Antwerp University Hospital and University of Antwerp, Belgium. “Research has shown that the elements of this pillar are highly predictive of injury severity and patient outcome.”

Biomarkers, imaging, modifiers offer critical clues to recovery

The second pillar uses biomarkers identified in blood tests to provide objective indicators of tissue damage, overcoming the limitations of clinical assessment that may inadvertently include symptoms unrelated to TBI.

Significantly, low levels of these biomarkers determine which patients do not require CT scans, reducing unnecessary radiation exposure and health care costs. These patients can then be discharged. In those with more severe injuries, CT and MRI imaging – the framework’s third pillar – are important in identifying blood clots, bleeding, and lesions that point to present and future symptoms.

Source: University of California – San Francisco

Categories : NeurologyTags :

Study Sheds Light on How Autistic People Communicate

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There is no significant difference in the effectiveness of how autistic and non-autistic people communicate, according to a new study, challenging the stereotype that autistic people struggle to connect with others.

The findings, published in Nature Human Behaviour, suggest that social difficulties often faced by autistic people are more about differences in how autistic and non-autistic people communicate, rather than a lack of social ability in autistic individuals, experts say. 

Researchers hope the results of the study will help reduce the stigma surrounding autism, and lead to more effective communication support for autistic people.  

Direct communication

Autism is a lifelong neurodivergence and disability, and influences how people experience and interact with the world. 

Autistic people often communicate more directly and may struggle with reading social cues and body language, leading to differences in how they engage in conversation compared to non-autistic people. 

Story sharing

The study, led by experts from the University of Edinburgh, tested how effectively information was passed between 311 autistic and non-autistic people. 

Participants were tested in groups where everyone was autistic, everyone was non-autistic, or a combination of both. 

The first person in the group heard a story from the researcher, then passed it along to the next person. Each person had to remember and repeat the story, and the last person in the chain recalled the story aloud. 

The amount of information passed on at each point in the chain was scored to discern how effective participants were at sharing the story. Researchers found there were no differences between autistic, non-autistic, and mixed groups.  

Increased awareness

After the task, participants rated how much they enjoyed the interaction with the other participants, based on how friendly, easy, or awkward the exchange was.  

Researchers found that non-autistic people preferred interacting with others like themselves, and autistic people preferred learning from fellow autistic individuals. This is likely down to the different ways that autistic and non-autistic people communicate, experts say.  

The findings confirm similar findings from a previous smaller study undertaken by the same researchers. They say the new evidence should lead to increased understanding of autistic communication styles as a difference, not a deficiency.   

Autism has often been associated with social impairments, both colloquially and in clinical criteria. Researchers have spent a lot of time trying to ‘fix’ autistic communication, but this study shows that despite autistic and non-autistic people communicating differently it is just as successful. With opportunities for autistic people often limited by misconceptions and misunderstandings, this new research could lead the way to bridging the communication gap and create more inclusive spaces for all.

 Dr Catherine Crompton, Chancellor’s Fellow at the University of Edinburgh’s Centre for Clinical Brain Sciences