. Scientific Frontline: Neuroscience
Showing posts with label Neuroscience. Show all posts
Showing posts with label Neuroscience. Show all posts

Wednesday, November 16, 2022

NIH researchers unlock pattern of gene activity for ADHD

A new study uses postmortem brain tissues to understand genomic differences in individuals with attention deficit hyperactivity disorder.
Image Credit: Gerd Altmann

Researchers at the National Institutes of Health have successfully identified differences in gene activity in the brains of people with attention deficit hyperactivity disorder (ADHD). The study, led by scientists at the National Human Genome Research Institute (NHGRI), part of NIH, found that individuals diagnosed with ADHD had differences in genes that code for known chemicals that brain cells use to communicate. The results of the findings, published in Molecular Psychiatry, show how genomic differences might contribute to symptoms.

To date, this is the first study to use postmortem human brain tissue to investigate ADHD. Other approaches to studying mental health conditions include non-invasively scanning the brain, which allows researchers to examine the structure and activation of brain areas. However, these studies lack information at the level of genes and how they might influence cell function and give rise to symptoms.

The researchers used a genomic technique called RNA sequencing to probe how specific genes are turned on or off, also known as gene expression. They studied two connected brain regions associated with ADHD: the caudate and the frontal cortex. These regions are known to be critical in controlling a person’s attention. Previous research found differences in the structure and activity of these brain regions in individuals with ADHD.

Tuesday, November 15, 2022

Solving brain dynamics gives rise to flexible machine-learning models

Studying the brains of small species recently helped MIT researchers better model the interaction between neurons and synapses — the building blocks of natural and artificial neural networks — into a class of flexible, robust machine-learning models that learn on the job and can adapt to changing conditions.
Image Credit: Ramin Hasani/Stable Diffusion

Last year, MIT researchers announced that they had built “liquid” neural networks, inspired by the brains of small species: a class of flexible, robust machine learning models that learn on the job and can adapt to changing conditions, for real-world safety-critical tasks, like driving and flying. The flexibility of these “liquid” neural nets meant boosting the bloodline to our connected world, yielding better decision-making for many tasks involving time-series data, such as brain and heart monitoring, weather forecasting, and stock pricing.

But these models become computationally expensive as their number of neurons and synapses increase and require clunky computer programs to solve their underlying, complicated math. And all of this math, similar to many physical phenomena, becomes harder to solve with size, meaning computing lots of small steps to arrive at a solution.

Now, the same team of scientists has discovered a way to alleviate this bottleneck by solving the differential equation behind the interaction of two neurons through synapses to unlock a new type of fast and efficient artificial intelligence algorithms. These modes have the same characteristics of liquid neural nets — flexible, causal, robust, and explainable — but are orders of magnitude faster, and scalable. This type of neural net could therefore be used for any task that involves getting insight into data over time, as they’re compact and adaptable even after training — while many traditional models are fixed.

Monday, November 14, 2022

The hunt for disrupted brain signals behind autism

The researchers delete one copy of a gene in specific neurons in mice to examine where circuit changes go wrong in ways that could lead to symptoms associated with autism.
Image Credit: National Institutes of Health

Part of understanding the underlying causes of autism spectrum disorder relies on figuring out which cells’ signaling patterns in the brain are disrupted, and when during nervous system development the disruption occurs.

New research findings in mouse models of one genetic risk for autism support the idea that loss of a specific gene interferes with cells in the brain whose role is to inhibit signaling. Though there are fewer of these cells than other neurons and their signals don’t travel very far, they have enormous influence on patterns of information transmission within the brain and to the rest of the body.

Ohio State University researchers found that deleting a copy of the autism-risk gene Arid1b from specific brain cells decreased the number of inhibitory cells and lowered signaling between inhibitory cells and the excitatory cells they help control. Previous research has suggested reduced inhibitory signals in mouse models of the disorder result in a range of autism-related behaviors.

In separate experiments, the scientists found that signaling changes linked to inhibitory cells can be seen in the same genetic mouse models of autism spectrum disorder (ASD) very shortly after birth, but the disruption might not be strong enough to interfere with normal brain development powered by a host of other genes.

Friday, November 11, 2022

Alzheimer's disease can be diagnosed before symptoms emerge

Oskar Hansson, Professor of Neurology Lund University 
Photo Credit: Kennet Ruona

A large study led by Lund University in Sweden has shown that people with Alzheimer's disease can now be identified before they experience any symptoms. It is now also possible to predict who will deteriorate within the next few years. The study is published in Nature Medicine, and is very timely in light of the recent development of new drugs for Alzheimer's disease.

It has long been known that there are two proteins linked to Alzheimer’s – beta-amyloid, which forms plaques in the brain, and tau, which at a later stage accumulates inside brain cells. Elevated levels of these proteins in combination with cognitive impairment have previously formed the basis for diagnosing Alzheimer's.

“Changes occur in the brain between ten and twenty years before the patient experiences any clear symptoms, and it is only when tau begins to spread that the nerve cells die and the person in question experiences the first cognitive problems. This is why Alzheimer's is so difficult to diagnose in its early stages”, explains Oskar Hansson, senior physician in neurology at Skåne University Hospital and professor at Lund University.

He has now led a large international research study that was carried out with 1,325 participants from Sweden, the US, the Netherlands and Australia. The participants did not have any cognitive impairment at the beginning of the study. By using PET scans, the presence of tau and amyloid in the participants' brains could be visualized. The people in whom the two proteins were discovered were found to be at a 20-40 times higher risk of developing the disease at follow-up a few years later, compared to the participants who had no biological changes.

Breathing may measurably modulate neural responses across brain

Wenyu Tu, co-author on the eLife paper and doctoral student in neuroscience in the Huck Institutes of the Life Sciences, sets up a functional MRI experiment. Functional MRI was used in conjunction with neuronal electrophysiology to identify a link between respiration and neural activity changes.
Photo Credit: Kelby Hochreither/Penn State

Mental health practitioners and meditation gurus have long credited intentional breathing with the ability to induce inner calm, but scientists do not fully understand how the brain is involved in the process. Using functional magnetic resonance imaging (fMRI) and electrophysiology, researchers in the Penn State College of Engineering identified a potential link between respiration and neural activity changes in rats.

Their results were made available online ahead of publication in eLife. The researchers used simultaneous multi-modal techniques to clear the noise typically associated with brain imaging and pinpoint where breathing regulated neural activity.

“There are roughly a million papers published on fMRI — a non-invasive imaging technique that allows researchers to examine brain activity in real time,” said Nanyin Zhang, founding director of the Penn State Center for Neurotechnology in Mental Health Research and professor of biomedical engineering. “Imaging researchers used to believe that respiration is a non-neural physiological artifact, like a heartbeat or body movement, in fMRI imaging. Our paper introduces the idea that respiration has a neural component: It affects the fMRI signal by modulating neural activity.”

By scanning the brainwaves of rodents in a resting state under anesthesia using fMRI, researchers revealed a network of brain regions involved in respiration.

Thursday, November 10, 2022

Rejuvenated immune cells can improve clearance of toxic waste from brain

Alzheimer’s, Parkinson’s and many other neurodegenerative diseases are marked by damaging clusters of proteins in the brain. Scientists have expended enormous effort searching for ways to treat such conditions by clearing these toxic clusters but have had limited success.

Now, researchers at Washington University School of Medicine in St. Louis has found an innovative way to improve waste clearance from the brain, and thereby possibly treat or even prevent neurodegenerative conditions. They showed that immune cells surrounding the brain influence how efficiently waste is swept out of the brain, and that such immune cells are impaired in old mice, and in people and mice with Alzheimer’s disease. Further, they found that treating old mice with an immune-stimulating compound rejuvenates immune cells and improves waste clearance from the brain.

The findings, published Nov. 9 in Nature, suggest a new approach to halting some of the effects of aging on the brain.

“Alzheimer’s has been studied for many years from the perspective of how neurons die, but there are other cells, such as immune cells on the periphery of the brain, that also may play a role in Alzheimer’s,” said senior author Jonathan Kipnis, PhD, the Alan A. and Edith L. Wolff Distinguished Professor of Pathology & Immunology and a BJC Investigator. “It doesn’t look likely that we will be able to revive dead or dying neurons, but the immune cells that sit on the borders of the brain are a feasible target for treating age-related brain diseases. They’re more accessible, and could be drugged or replaced. In this study, we treated aged mice with a molecule that can activate aged immune cells, and it worked in improving fluid flow and waste clearance from the brain. This holds promise as an approach to treating neurodegenerative diseases.”

Tuesday, November 8, 2022

UQ study explains link between sleep apnea and dementia

Professor Elizabeth Coulson said the findings suggest CPAP treatment of obstructive sleep apnea has the potential to reduce dementia risk.
Credit: University of Queensland

Researchers at The University of Queensland have discovered a link between obstructive sleep apnea and an increased risk of developing dementia.

Professor Elizabeth Coulson from UQ’s Queensland Brain Institute and School of Biomedical Sciences and her team found a causal relationship between a lack of oxygen to the brain during sleep and Alzheimer’s disease in mice.

“We found sleep deprivation alone in mice caused only mild cognitive impairment,” Professor Coulson said.

“But we developed a novel way to induce sleep-disrupted breathing and found the mice displayed exacerbated pathological features of Alzheimer’s disease.

“It demonstrated that hypoxia – when the brain is deprived of oxygen – caused the same selective degeneration of neurons that characteristically die in dementia.”

Professor Coulson said the next step would be to determine what levels of hypoxia result in brain degeneration in humans.

Study shows differences between brains of primates — humans, apes and monkeys — are small but significant

Researchers analyzed genetic material from cells in the prefrontal cortex (the area shaded in each brain) from four closely-related primates to characterize subtle differences in cell type and genetics.
Source/Credit: University of Wisconsin–Madison

While the physical differences between humans and non-human primates are quite distinct, a new study reveals their brains may be remarkably similar. And yet, the smallest changes may make big differences in developmental and psychiatric disorders.

Understanding the molecular differences that make the human brain distinct can help researchers study disruptions in its development. A new study, published recently in the journal Science by a team including University of Wisconsin–Madison neuroscience professor Andre Sousa, investigates the differences and similarities of cells in the prefrontal cortex — the frontmost region of the brain, an area that plays a central role in higher cognitive functions — between humans and non-human primates such as chimpanzees, Rhesus macaques and marmosets.

The cellular differences between these species may illuminate steps in their evolution and how those differences can be implicated in disorders, such as autism and intellectual disabilities, seen in humans. Sousa, who studies the developmental biology of the brain at UW–Madison’s Waisman Center, decided to start by studying and categorizing the cells in the prefrontal cortex in partnership with the Yale University lab where he worked as a postdoctoral researcher.

New experimental treatment can stop the growth of schwannoma tumors

Researchers showed that after just 21 days of the drugs being administered, tumor growth can be strongly and significantly reduced.

Two novel and orally administered drugs can not only block the growth, but also shrink the size, of a tumor type found in the nervous system, new research has shown.

The tumors, schwannomas, most frequently grow on the nerves that bring hearing and balance information into the brain. Schwannomas are the most common nerve sheath tumor, and can occur in anyone but are also linked to a hereditary condition known as Neurofibromatosis Type II (NF2).

In NF2, where the function of the protein Merlin is lost in cells, patients frequently develop not only schwannomas, but also meningioma tumors associated with the brain and spinal cord.

The treatment of both tumor types is difficult, with surgery being the current mainstay but also carrying a high risk of damage to the surrounding normal nervous system tissue.

With an urgent need for new treatments, an international team of scientists focused on the Hippo signaling pathway, which normally controls organ size in human tissues and cells, but is dysregulated in multiple types of cancer.

Monday, November 7, 2022

A Brain Stimulator That Powers with Breath Instead of Batteries

UConn researchers have developed a way of charging deep brain stimulators that don't require the battery power that's currently standard
Credit/Source: University of Connecticut Contributed Illustration

Implantable deep brain stimulators can help many people with neurological and psychiatric disease when traditional treatments fail. But surgery every time the batteries need to be changed is a major drawback. Now, UConn researchers report in Cell Reports Physical Sciences a new way to charge the devices using a person’s own breathing movements.

Deep brain stimulators are becoming more common, with about 150,000 new devices implanted each year. They are normally placed under the skin in the chest area and their electrodes implanted within the brain. The electrodes zap the brain with electrical pulses multiple times per second to regulate the brain’s abnormal electrical activity. Deep brain stimulators can help people with Parkinson’s disease and other movement disorders to regain control over their muscle motions. Research has also shown the technique can significantly reduce the symptoms for psychiatric conditions such as treatment-resistant depression and obsessive-compulsive disorder.

Just like a pacemaker, deep brain stimulators are battery powered. While most pacemaker batteries last from 7-10 years, deep brain stimulator batteries typically require changing every 2-3 years because of their high energy consumption. And each battery change requires surgery.

UConn chemists Esraa Elsanadidy, Islam Mosa, James Rusling, and their collaborators have developed a deep brain stimulator that never needs its batteries changed.

Friday, November 4, 2022

Characterizing the ‘Noisy Life of a Musician’: Risks and Benefits for Brain Aging

Skoe's study will gather information about participants' noise environments, both while playing music and doing other daily activities.
Credit: Pixabay

As a child growing up in Germany, Erika Skoe taught herself to play German songs on the piano before she was comfortable speaking the language. Skoe, now an associate professor of speech, language, and hearing sciences at UConn and self-described lapsed musician has made a career studying hearing and brain function in people young to old, with a special focus on language and music.

Previous research has shown that regular exposure to noise may accelerate brain aging. But other work shows older musicians’ brain and cognitive function resembles that of somebody much younger. To Skoe, these independent lines of research seemed at odds: if noise exposure is harmful to the brain, why are older musicians neurologically sharper than non-musicians, given that musicians are at higher risk of experiencing dangerous noise levels?

In a new $1.6 million grant from the National Institutes of Health, titled “The Noisy Life of the Musician: Implications for Healthy Brain Aging,” Skoe will lead an effort to reconcile the health benefits and hazards of being a musician and their interplay as people age. This study was funded through the NIH Sound Health initiative, a program supporting research on health applications of music.

New View on the Brain: It’s All in the Connections

Source: Radboud University Nijmegen

It’s not the individual brain regions but rather their connections that matter: neuroscientists propose a new model of how the brain works. This new view enables us to understand better why and how our brains vary between individuals. The researchers published it in a special issue of Science on November 4th.

Our right hemisphere is for creativity, and the left is for rational thinking. It’s an urban myth that stems from a classical view of how our brain works, namely that we have several brain regions that all have a specific function. Even though this ‘modular’ view of the brain is superseded, it can still be found in many textbooks.

However, we should look at brain function differently, according to neuroscientists Stephanie Forkel at Radboud University and Michel Thiebaut de Schotten at the University of Bordeaux. Brain functions are not localized in individual brain regions but rather emerge from the exchange between these regions.

Thursday, November 3, 2022

Association between poor sleep quality and an increased risk of developing Alzheimer's

Photo Credit: Claudio_Scott
New research has shown an association between sleep quality – less than seven hours - and Alzheimer's disease-related pathology in people without cognitive impairment. The study by an international team led by the Pasqual Maragall Foundation research centre, the Barcelonaβeta Brain Research Centre (BBRC), together with researchers from the University of Bristol and North Bristol NHS Trust, is published in the scientific journal Brain Communications today [3 November].

The results of the analysis, part of the European Prevention of Alzheimer's Dementia Longitudinal Cohort Study (EPAD LCS), indicate that poor sleep quality is related to an increase in pathology of Alzheimer's disease. This finding is relevant to help define future therapies, so that they can be targeted at the appropriate phase of the disease.

A cross-sectional analysis of sleep quality

Sleep abnormalities are common in Alzheimer's disease, and sleep quality can be affected early in the preclinical stage of the disease, even when no other symptoms are experienced. Understanding how and when sleep deprivation contributes to Alzheimer's disease progression is important for the design and implementation of future therapies.

Laura Stankeviciute, a predoctoral researcher at the BBRC and one of the main authors of the study, said: "The epidemiological and experimental data available to date already suggested that sleep abnormalities contribute to the risk of Alzheimer's disease.

"However, previous studies had limitations due to the lack of biomarkers of Alzheimer's disease, because they had a non-cross-sectional design, or because of the small size of the sample of participants.” This is the first study to include all of these factors.

Wednesday, November 2, 2022

Study urges caution when comparing neural networks to the brain

Neural networks, a type of computing system loosely modeled on the organization of the human brain, form the basis of many artificial intelligence systems for applications such speech recognition, computer vision, and medical image analysis.
Image Credits: Christine Daniloff | Massachusetts Institute of Technology

Neural networks, a type of computing system loosely modeled on the organization of the human brain, form the basis of many artificial intelligence systems for applications such speech recognition, computer vision, and medical image analysis.

In the field of neuroscience, researchers often use neural networks to try to model the same kind of tasks that the brain performs, in hopes that the models could suggest new hypotheses regarding how the brain itself performs those tasks. However, a group of researchers at MIT is urging that more caution should be taken when interpreting these models.

In an analysis of more than 11,000 neural networks that were trained to simulate the function of grid cells — key components of the brain’s navigation system — the researchers found that neural networks only produced grid-cell-like activity when they were given very specific constraints that are not found in biological systems.

“What this suggests is that in order to obtain a result with grid cells, the researchers training the models needed to bake in those results with specific, biologically implausible implementation choices,” says Rylan Schaeffer, a former senior research associate at MIT.

Daytime Naps Reinforce Memories of Emotional Trauma and Anxiety

According to Yuri Pavlov, the positive effect of sleep on memory can be observed years later.
Photo Credit: Nadezhda Pavlova

Scientists from Ural Federal University and the University of Tübingen (Germany) studied the effect of sleep on the formation and translation of primary memories of something scary into long-term memory. Neurobiologists discovered that sleeping during the day strengthens memory of disturbing and frightening events, but a similar effect of memory strengthening is also observed after a period of calm wakefulness. The findings will be useful for developing rehabilitation strategies for people who have been emotionally traumatized by disasters, warfare, and violence. The study was published in the journal Cognitive, Affective, & Behavioral Neuroscience.

Memory consolidation - the transition of memories from short-term memory to long-term memory - occurs primarily during sleep. Studies show that sleep after learning can have positive effects that are superior to passive wakefulness. This occurs by reactivating important memories, which may also be reflected in dreams. The positive effects of dreaming can be observed even years later. However, there are currently no studies that analyze whether sleep enhances the effect of remembering emotionally difficult events. Therefore, scientists decided to find out how sleep affects the memory of a person's experience of fear.

Tuesday, November 1, 2022

‘A silent killer’ - COVID-19 shown to trigger inflammation in the brain

A COVID-19 infected mouse brain showing 'angry' microglia in green and SARS-CoV-2 in red.
Source/Credit: University of Queensland

Research led by The University of Queensland has found COVID-19 activates the same inflammatory response in the brain as Parkinson’s disease.

The discovery identified a potential future risk for neurodegenerative conditions in people who’ve had COVID-19, but also a possible treatment.

The UQ team was led by Professor Trent Woodruff and Dr Eduardo Albornoz Balmaceda from UQ’s School of Biomedical Sciences, and virologists from the School of Chemistry and Molecular Biosciences.

“We studied the effect of the virus on the brain’s immune cells, ‘microglia’ which are the key cells involved in the progression of brain diseases like Parkinson’s and Alzheimer’s,” Professor Woodruff said.

“Our team grew human microglia in the laboratory and infected the cells with SARS-CoV-2, the virus that causes COVID-19.

“We found the cells effectively became ‘angry’, activating the same pathway that Parkinson’s and Alzheimer’s proteins can activate in disease, the inflammasomes.”

Wednesday, October 26, 2022

Awareness of one’s own body is based on uncertainty and guesses

Researchers at Karolinska Institutet have found that the perception of one's own body is very based on the brain making guesses based on probability theory. It shows a study recently published in the journal eLife.

How we perceive our own body is largely based on probability assessments based on past experiences, in combination with sensory information such as vision and feeling, for example.

You could say that the experience of your own body is a statistical estimate of reality based on sensory information, sensorory uncertainty, and past experiences that can be summed up in the mathematical model explain Henrik Ehrsson, professor at the Department of Neuroscience, Karolinska Institutet.

Monday, October 24, 2022

Study looks inside the brain during sleep to show how memory is stored


MRI scans showing locations of medial-temporal electrodes in a representative patient.
Source/Credit: Department of Neurological Surgery, The University of Chicago.

A new study looks deep inside the brain, where previous learning was reactivated during sleep, resulting in improved memory.

Neuroscientists from Northwestern University teamed up with clinicians from the University of Chicago Epilepsy Center to study the brain electrical activity in five of the center’s patients in response to sounds administered by the research team as part of a learning exercise.

The five patients who volunteered to participate in the study had electrode probes implanted into the brain for the purpose of investigating potential treatments for their seizure disorders.

While prior studies have used EEG recordings captured by electrodes on the head to measure memory processing during sleep, this is the first study to record such electrical activity from inside the brain.

The study found participants significantly improved their performance in a recall test the next morning. The mapped brain activity allowed the researchers to take a big step forward in understanding how memory storage works by providing visual data identifying the areas of the brain engaged in the process of overnight memory storage.

Gestational Exposure to Flame Retardant Alters Brain Development in Rats

A new study from North Carolina State University shows that exposure in utero to the flame retardant FireMaster® 550 (FM 550), or to its individual brominated (BFR) or organophosphate ester (OPFR) components, resulted in altered brain development in newborn rats. The effects – most notably evidence of mitochondrial disruption and dysregulated choline and triglyceride levels in brain tissue – were greater in male offspring than in females. The work adds to the body of evidence that both OPFRs and BFRs can be neurotoxic.

FM 550 is a flame-retardant mixture first identified a decade ago. It was developed to replace PBDEs, a class of fire retardants being phased out due to safety concerns.

“While some new flame-retardant mixtures still contain BFRs, the OPFRs are a popular substitute for PBDEs, since it is believed that OPFRs don’t accumulate in the body and thus cannot be as harmful,” says Heather Patisaul, associate dean for research in NC State’s College of Sciences and corresponding author of the study. “Specifically, it was thought that OPFRs wouldn’t impact acetylcholinesterase – a key neurotransmitter. But it looks as though OPFRs still impact choline signaling and are just as bad if not worse than PBDEs for the developing brain.”

Patisaul and her colleagues performed transcriptomic and lipidomic studies on the prefrontal cortexes of newborn rats whose mothers had been exposed to FM550, or to BFR or OPFR elements individually, during gestation.

Microscopy reveals how psychedelics light up brain’s neuropathways

 Alex Kwan, Ph.D. ‘09, associate professor in the Meinig School of Biomedical Engineering, is using optical microscopy and other tools to map the brain’s neural response to psychedelic drugs, an approach that could lead to the development of fast-acting antidepressants
Photo credit: Ryan Young/Cornell University.

What a long, strange trip it’s been for psychedelic drugs. From their use in ancient indigenous ceremonies, to their often-caricatured association with the 1960s counterculture, to their recent reemergence as a potential therapeutic, hallucinogens have been embraced by very different communities for very different reasons. But scientists have never fully understood how these drugs actually work on the brain.

Alex Kwan, Ph.D. ‘09, associate professor in the Meinig School of Biomedical Engineering in the College of Engineering, is using optical microscopy and other tools to map the brain’s neural response to these psychoactive chemicals, an approach that could eventually lead to the development of fast-acting antidepressants and treatments for substance-use disorders and cluster headaches.

“We know more about the pharmacology, how psychedelics work at the structural level, interacting with the brain receptors. But there has been a big void in terms of understanding what they do to the brain itself, at the neural circuit level,” Kwan said. “There’s a chain of events that happen that ultimately lead to acute and longer-lasting behavioral changes that might be useful for treatment. But in between a lot of that is a black box.”

Despite the renewed interest in the benefits of psychedelics from popular figures such as environmentalist and author Michael Pollan, much of the research into these drugs was conducted in the 1950s and 60s with fairly rudimentary methods, Kwan said.

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